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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Circadian rhythms, Wnt/beta-catenin pathway and PPAR alpha/gamma profiles in diseases with primary or secondary cardiac dysfunction</title><author><name sortKey="Lecarpentier, Yves" sort="Lecarpentier, Yves" uniqKey="Lecarpentier Y" first="Yves" last="Lecarpentier">Yves Lecarpentier</name><affiliation><nlm:aff id="aff1"><institution>Centre de Recherche Clinique, Centre Hospitalier Régional de Meaux</institution><country>Meaux, France</country></nlm:aff></affiliation></author><author><name sortKey="Claes, Victor" sort="Claes, Victor" uniqKey="Claes V" first="Victor" last="Claes">Victor Claes</name><affiliation><nlm:aff id="aff2"><institution>Department of Pharmaceutical Sciences, University of Antwerp</institution><country>Wilrijk, Belgium</country></nlm:aff></affiliation></author><author><name sortKey="Duthoit, Guillaume" sort="Duthoit, Guillaume" uniqKey="Duthoit G" first="Guillaume" last="Duthoit">Guillaume Duthoit</name><affiliation><nlm:aff id="aff3"><institution>Institut de Cardiologie, Hôpital de la Pitié-Salpêtière</institution><country>Paris, France</country></nlm:aff></affiliation></author><author><name sortKey="Hebert, Jean Louis" sort="Hebert, Jean Louis" uniqKey="Hebert J" first="Jean-Louis" last="Hébert">Jean-Louis Hébert</name><affiliation><nlm:aff id="aff3"><institution>Institut de Cardiologie, Hôpital de la Pitié-Salpêtière</institution><country>Paris, France</country></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25414671</idno><idno type="pmc">4220097</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220097</idno><idno type="RBID">PMC:4220097</idno><idno type="doi">10.3389/fphys.2014.00429</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000961</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000961</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Circadian rhythms, Wnt/beta-catenin pathway and PPAR alpha/gamma profiles in diseases with primary or secondary cardiac dysfunction</title><author><name sortKey="Lecarpentier, Yves" sort="Lecarpentier, Yves" uniqKey="Lecarpentier Y" first="Yves" last="Lecarpentier">Yves Lecarpentier</name><affiliation><nlm:aff id="aff1"><institution>Centre de Recherche Clinique, Centre Hospitalier Régional de Meaux</institution><country>Meaux, France</country></nlm:aff></affiliation></author><author><name sortKey="Claes, Victor" sort="Claes, Victor" uniqKey="Claes V" first="Victor" last="Claes">Victor Claes</name><affiliation><nlm:aff id="aff2"><institution>Department of Pharmaceutical Sciences, University of Antwerp</institution><country>Wilrijk, Belgium</country></nlm:aff></affiliation></author><author><name sortKey="Duthoit, Guillaume" sort="Duthoit, Guillaume" uniqKey="Duthoit G" first="Guillaume" last="Duthoit">Guillaume Duthoit</name><affiliation><nlm:aff id="aff3"><institution>Institut de Cardiologie, Hôpital de la Pitié-Salpêtière</institution><country>Paris, France</country></nlm:aff></affiliation></author><author><name sortKey="Hebert, Jean Louis" sort="Hebert, Jean Louis" uniqKey="Hebert J" first="Jean-Louis" last="Hébert">Jean-Louis Hébert</name><affiliation><nlm:aff id="aff3"><institution>Institut de Cardiologie, Hôpital de la Pitié-Salpêtière</institution><country>Paris, France</country></nlm:aff></affiliation></author></analytic><series><title level="j">Frontiers in Physiology</title><idno type="eISSN">1664-042X</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Circadian clock mechanisms are far-from-equilibrium dissipative structures. Peroxisome proliferator-activated receptors (PPAR alpha, beta/delta, and gamma) play a key role in metabolic regulatory processes, particularly in heart muscle. Links between circadian rhythms (CRs) and PPARs have been established. Mammalian CRs involve at least two critical transcription factors, CLOCK and BMAL1 (Gekakis et al., <xref rid="B51" ref-type="bibr">1998</xref>; Hogenesch et al., <xref rid="B70" ref-type="bibr">1998</xref>). PPAR gamma plays a major role in both glucose and lipid metabolisms and presents circadian properties which coordinate the interplay between metabolism and CRs. PPAR gamma is a major component of the vascular clock. Vascular PPAR gamma is a peripheral regulator of cardiovascular rhythms controlling circadian variations in blood pressure and heart rate through BMAL1. We focused our review on diseases with abnormalities of CRs and with primary or secondary cardiac dysfunction. Moreover, these diseases presented changes in the Wnt/beta-catenin pathway and PPARs, according to two opposed profiles. Profile 1 was defined as follows: inactivation of the Wnt/beta-catenin pathway with increased expression of PPAR gamma. Profile 2 was defined as follows: activation of the Wnt/beta-catenin pathway with decreased expression of PPAR gamma. A typical profile 1 disease is arrhythmogenic right ventricular cardiomyopathy, a genetic cardiac disease which presents mutations of the desmosomal proteins and is mainly characterized by fatty acid accumulation in adult cardiomyocytes mainly in the right ventricle. The link between PPAR gamma dysfunction and desmosomal genetic mutations occurs via inactivation of the Wnt/beta-catenin pathway presenting oscillatory properties. A typical profile 2 disease is type 2 diabetes, with activation of the Wnt/beta-catenin pathway and decreased expression of PPAR gamma. CRs abnormalities are present in numerous pathologies such as cardiovascular diseases, sympathetic/parasympathetic dysfunction, hypertension, diabetes, neurodegenerative diseases, cancer which are often closely inter-related.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Akashi, M" uniqKey="Akashi M">M. Akashi</name></author><author><name sortKey="Takumi, T" uniqKey="Takumi T">T. Takumi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Anan, F" uniqKey="Anan F">F. Anan</name></author><author><name sortKey="Masaki, T" uniqKey="Masaki T">T. Masaki</name></author><author><name sortKey="Fukunaga, N" uniqKey="Fukunaga N">N. Fukunaga</name></author><author><name sortKey="Teshima, Y" uniqKey="Teshima Y">Y. Teshima</name></author><author><name sortKey="Iwao, T" uniqKey="Iwao T">T. Iwao</name></author><author><name sortKey="Kaneda, K" uniqKey="Kaneda K">K. Kaneda</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Andreassen, O A" uniqKey="Andreassen O">O. A. Andreassen</name></author><author><name sortKey="Djurovic, S" uniqKey="Djurovic S">S. Djurovic</name></author><author><name sortKey="Thompson, W K" uniqKey="Thompson W">W. K. Thompson</name></author><author><name sortKey="Schork, A J" uniqKey="Schork A">A. J. Schork</name></author><author><name sortKey="Kendler, K S" uniqKey="Kendler K">K. S. Kendler</name></author><author><name sortKey="O Donovan, M C" uniqKey="O Donovan M">M. C. O'Donovan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Andrich, J" uniqKey="Andrich J">J. Andrich</name></author><author><name sortKey="Schmitz, T" uniqKey="Schmitz T">T. Schmitz</name></author><author><name sortKey="Saft, C" uniqKey="Saft C">C. Saft</name></author><author><name sortKey="Postert, T" uniqKey="Postert T">T. Postert</name></author><author><name sortKey="Kraus, P" uniqKey="Kraus P">P. Kraus</name></author><author><name sortKey="Epplen, J T" uniqKey="Epplen J">J. T. Epplen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Anea, C B" uniqKey="Anea C">C. B. Anea</name></author><author><name sortKey="Zhang, M" uniqKey="Zhang M">M. Zhang</name></author><author><name sortKey="Stepp, D W" uniqKey="Stepp D">D. W. Stepp</name></author><author><name sortKey="Simkins, G B" uniqKey="Simkins G">G. B. Simkins</name></author><author><name sortKey="Reed, G" uniqKey="Reed G">G. Reed</name></author><author><name sortKey="Fulton, D J" uniqKey="Fulton D">D. J. Fulton</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Aziz, N A" uniqKey="Aziz N">N. A. Aziz</name></author><author><name sortKey="Anguelova, G V" uniqKey="Anguelova G">G. V. Anguelova</name></author><author><name sortKey="Marinus, J" uniqKey="Marinus J">J. Marinus</name></author><author><name sortKey="Lammers, G J" uniqKey="Lammers G">G. J. Lammers</name></author><author><name sortKey="Roos, R A" uniqKey="Roos R">R. A. Roos</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Barger, P M" uniqKey="Barger P">P. M. Barger</name></author><author><name sortKey="Brandt, J M" uniqKey="Brandt J">J. M. Brandt</name></author><author><name sortKey="Leone, T C" uniqKey="Leone T">T. C. Leone</name></author><author><name sortKey="Weinheimer, C J" uniqKey="Weinheimer C">C. J. Weinheimer</name></author><author><name sortKey="Kelly, D P" uniqKey="Kelly D">D. P. Kelly</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Basso, C" uniqKey="Basso C">C. Basso</name></author><author><name sortKey="Corrado, D" uniqKey="Corrado D">D. Corrado</name></author><author><name sortKey="Marcus, F I" uniqKey="Marcus F">F. I. Marcus</name></author><author><name sortKey="Nava, A" uniqKey="Nava A">A. Nava</name></author><author><name sortKey="Thiene, G" uniqKey="Thiene G">G. Thiene</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Belanger, A J" uniqKey="Belanger A">A. J. Belanger</name></author><author><name sortKey="Lu, H" uniqKey="Lu H">H. Lu</name></author><author><name sortKey="Date, T" uniqKey="Date T">T. Date</name></author><author><name sortKey="Liu, L X" uniqKey="Liu L">L. X. Liu</name></author><author><name sortKey="Vincent, K A" uniqKey="Vincent K">K. A. Vincent</name></author><author><name sortKey="Akita, G Y" uniqKey="Akita G">G. Y. Akita</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Benedusi, V" uniqKey="Benedusi V">V. Benedusi</name></author><author><name sortKey="Martorana, F" uniqKey="Martorana F">F. Martorana</name></author><author><name sortKey="Brambilla, L" uniqKey="Brambilla L">L. Brambilla</name></author><author><name sortKey="Maggi, A" uniqKey="Maggi A">A. Maggi</name></author><author><name sortKey="Rossi, D" uniqKey="Rossi D">D. Rossi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ben Ze Ev, A" uniqKey="Ben Ze Ev A">A. Ben-Ze'ev</name></author><author><name sortKey="Geiger, B" uniqKey="Geiger B">B. Geiger</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Berger, J" uniqKey="Berger J">J. Berger</name></author><author><name sortKey="Moller, D E" uniqKey="Moller D">D. E. Moller</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Boonen, R A" uniqKey="Boonen R">R. A. Boonen</name></author><author><name sortKey="Van Tijn, P" uniqKey="Van Tijn P">P. van Tijn</name></author><author><name sortKey="Zivkovic, D" uniqKey="Zivkovic D">D. Zivkovic</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Brack, A S" uniqKey="Brack A">A. S. Brack</name></author><author><name sortKey="Conboy, M J" uniqKey="Conboy M">M. J. Conboy</name></author><author><name sortKey="Roy, S" uniqKey="Roy S">S. Roy</name></author><author><name sortKey="Lee, M" uniqKey="Lee M">M. Lee</name></author><author><name sortKey="Kuo, C J" uniqKey="Kuo C">C. J. Kuo</name></author><author><name sortKey="Keller, C" uniqKey="Keller C">C. Keller</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bray, M S" uniqKey="Bray M">M. S. Bray</name></author><author><name sortKey="Shaw, C A" uniqKey="Shaw C">C. A. Shaw</name></author><author><name sortKey="Moore, M W" uniqKey="Moore M">M. W. Moore</name></author><author><name sortKey="Garcia, R A" uniqKey="Garcia R">R. A. Garcia</name></author><author><name sortKey="Zanquetta, M M" uniqKey="Zanquetta M">M. M. Zanquetta</name></author><author><name sortKey="Durgan, D J" uniqKey="Durgan D">D. J. Durgan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Breen, D P" uniqKey="Breen D">D. P. Breen</name></author><author><name sortKey="Vuono, R" uniqKey="Vuono R">R. Vuono</name></author><author><name sortKey="Nawarathna, U" uniqKey="Nawarathna U">U. Nawarathna</name></author><author><name sortKey="Fisher, K" uniqKey="Fisher K">K. Fisher</name></author><author><name sortKey="Shneerson, J M" uniqKey="Shneerson J">J. M. Shneerson</name></author><author><name sortKey="Reddy, A B" uniqKey="Reddy A">A. B. Reddy</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cai, Y" uniqKey="Cai Y">Y. Cai</name></author><author><name sortKey="Liu, S" uniqKey="Liu S">S. Liu</name></author><author><name sortKey="Sothern, R B" uniqKey="Sothern R">R. B. Sothern</name></author><author><name sortKey="Xu, S" uniqKey="Xu S">S. Xu</name></author><author><name sortKey="Chan, P" uniqKey="Chan P">P. Chan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Canalis, E" uniqKey="Canalis E">E. Canalis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Canaple, L" uniqKey="Canaple L">L. Canaple</name></author><author><name sortKey="Rambaud, J" uniqKey="Rambaud J">J. Rambaud</name></author><author><name sortKey="Dkhissi Benyahya, O" uniqKey="Dkhissi Benyahya O">O. Dkhissi-Benyahya</name></author><author><name sortKey="Rayet, B" uniqKey="Rayet B">B. Rayet</name></author><author><name sortKey="Tan, N S" uniqKey="Tan N">N. S. Tan</name></author><author><name sortKey="Michalik, L" uniqKey="Michalik L">L. Michalik</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cermakian, N" uniqKey="Cermakian N">N. Cermakian</name></author><author><name sortKey="Lamont, E W" uniqKey="Lamont E">E. W. Lamont</name></author><author><name sortKey="Boudreau, P" uniqKey="Boudreau P">P. Boudreau</name></author><author><name sortKey="Boivin, D B" uniqKey="Boivin D">D. B. Boivin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chan, A O" uniqKey="Chan A">A. O. Chan</name></author><author><name sortKey="Jim, M H" uniqKey="Jim M">M. H. Jim</name></author><author><name sortKey="Lam, K F" uniqKey="Lam K">K. F. Lam</name></author><author><name sortKey="Morris, J S" uniqKey="Morris J">J. S. Morris</name></author><author><name sortKey="Siu, D C" uniqKey="Siu D">D. C. Siu</name></author><author><name sortKey="Tong, T" uniqKey="Tong T">T. Tong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chatterjee, S" uniqKey="Chatterjee S">S. Chatterjee</name></author><author><name sortKey="Nam, D" uniqKey="Nam D">D. Nam</name></author><author><name sortKey="Guo, B" uniqKey="Guo B">B. Guo</name></author><author><name sortKey="Kim, J M" uniqKey="Kim J">J. M. Kim</name></author><author><name sortKey="Winnier, G E" uniqKey="Winnier G">G. E. Winnier</name></author><author><name sortKey="Lee, J" uniqKey="Lee J">J. Lee</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chen, L" uniqKey="Chen L">L. Chen</name></author><author><name sortKey="Yang, G" uniqKey="Yang G">G. Yang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Clevers, H" uniqKey="Clevers H">H. Clevers</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Clevers, H" uniqKey="Clevers H">H. Clevers</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Clevers, H" uniqKey="Clevers H">H. Clevers</name></author><author><name sortKey="Batlle, E" uniqKey="Batlle E">E. Batlle</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Coppola, G" uniqKey="Coppola G">G. Coppola</name></author><author><name sortKey="Marmolino, D" uniqKey="Marmolino D">D. Marmolino</name></author><author><name sortKey="Lu, D" uniqKey="Lu D">D. Lu</name></author><author><name sortKey="Wang, Q" uniqKey="Wang Q">Q. Wang</name></author><author><name sortKey="Cnop, M" uniqKey="Cnop M">M. Cnop</name></author><author><name sortKey="Rai, M" uniqKey="Rai M">M. Rai</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Corrado, D" uniqKey="Corrado D">D. Corrado</name></author><author><name sortKey="Basso, C" uniqKey="Basso C">C. Basso</name></author><author><name sortKey="Thiene, G" uniqKey="Thiene G">G. Thiene</name></author><author><name sortKey="Mckenna, W J" uniqKey="Mckenna W">W. J. McKenna</name></author><author><name sortKey="Davies, M J" uniqKey="Davies M">M. J. Davies</name></author><author><name sortKey="Fontaliran, F" uniqKey="Fontaliran F">F. Fontaliran</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Curtis, A M" uniqKey="Curtis A">A. M. Curtis</name></author><author><name sortKey="Cheng, Y" uniqKey="Cheng Y">Y. Cheng</name></author><author><name sortKey="Kapoor, S" uniqKey="Kapoor S">S. Kapoor</name></author><author><name sortKey="Reilly, D" uniqKey="Reilly D">D. Reilly</name></author><author><name sortKey="Price, T S" uniqKey="Price T">T. S. Price</name></author><author><name sortKey="Fitzgerald, G A" uniqKey="Fitzgerald G">G. A. Fitzgerald</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="De Ferrari, G" uniqKey="De Ferrari G">G. De Ferrari</name></author><author><name sortKey="Avila, M" uniqKey="Avila M">M. Avila</name></author><author><name sortKey="Medina, M" uniqKey="Medina M">M. Medina</name></author><author><name sortKey="Perez Palma, E" uniqKey="Perez Palma E">E. Perez-Palma</name></author><author><name sortKey="Bustos, B" uniqKey="Bustos B">B. Bustos</name></author><author><name sortKey="Alarcon, M" uniqKey="Alarcon M">M. Alarcon</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Desjardins, F" uniqKey="Desjardins F">F. Desjardins</name></author><author><name sortKey="Sekkali, B" uniqKey="Sekkali B">B. Sekkali</name></author><author><name sortKey="Verreth, W" uniqKey="Verreth W">W. Verreth</name></author><author><name sortKey="Pelat, M" uniqKey="Pelat M">M. Pelat</name></author><author><name sortKey="De Keyzer, D" uniqKey="De Keyzer D">D. De Keyzer</name></author><author><name sortKey="Mertens, A" uniqKey="Mertens A">A. Mertens</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Djouadi, F" uniqKey="Djouadi F">F. Djouadi</name></author><author><name sortKey="Lecarpentier, Y" uniqKey="Lecarpentier Y">Y. Lecarpentier</name></author><author><name sortKey="Hebert, J L" uniqKey="Hebert J">J. L. Hebert</name></author><author><name sortKey="Charron, P" uniqKey="Charron P">P. Charron</name></author><author><name sortKey="Bastin, J" uniqKey="Bastin J">J. Bastin</name></author><author><name sortKey="Coirault, C" uniqKey="Coirault C">C. Coirault</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Drew, P D" uniqKey="Drew P">P. D. Drew</name></author><author><name sortKey="Xu, J" uniqKey="Xu J">J. Xu</name></author><author><name sortKey="Racke, M K" uniqKey="Racke M">M. K. Racke</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Druschky, A" uniqKey="Druschky A">A. Druschky</name></author><author><name sortKey="Spitzer, A" uniqKey="Spitzer A">A. Spitzer</name></author><author><name sortKey="Platsch, G" uniqKey="Platsch G">G. Platsch</name></author><author><name sortKey="Claus, D" uniqKey="Claus D">D. Claus</name></author><author><name sortKey="Feistel, H" uniqKey="Feistel H">H. Feistel</name></author><author><name sortKey="Druschky, K" uniqKey="Druschky K">K. Druschky</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dupont, P" uniqKey="Dupont P">P. Dupont</name></author><author><name sortKey="Besson, M T" uniqKey="Besson M">M. T. Besson</name></author><author><name sortKey="Devaux, J" uniqKey="Devaux J">J. Devaux</name></author><author><name sortKey="Lievens, J C" uniqKey="Lievens J">J. C. Lievens</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Duque, G" uniqKey="Duque G">G. Duque</name></author><author><name sortKey="Li, W" uniqKey="Li W">W. Li</name></author><author><name sortKey="Vidal, C" uniqKey="Vidal C">C. Vidal</name></author><author><name sortKey="Bermeo, S" uniqKey="Bermeo S">S. Bermeo</name></author><author><name sortKey="Rivas, D" uniqKey="Rivas D">D. Rivas</name></author><author><name sortKey="Henderson, J" uniqKey="Henderson J">J. Henderson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Durgan, D J" uniqKey="Durgan D">D. J. Durgan</name></author><author><name sortKey="Hotze, M A" uniqKey="Hotze M">M. A. Hotze</name></author><author><name sortKey="Tomlin, T M" uniqKey="Tomlin T">T. M. Tomlin</name></author><author><name sortKey="Egbejimi, O" uniqKey="Egbejimi O">O. Egbejimi</name></author><author><name sortKey="Graveleau, C" uniqKey="Graveleau C">C. Graveleau</name></author><author><name sortKey="Abel, E D" uniqKey="Abel E">E. D. Abel</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Durgan, D J" uniqKey="Durgan D">D. J. Durgan</name></author><author><name sortKey="Moore, M W" uniqKey="Moore M">M. W. Moore</name></author><author><name sortKey="Ha, N P" uniqKey="Ha N">N. P. Ha</name></author><author><name sortKey="Egbejimi, O" uniqKey="Egbejimi O">O. Egbejimi</name></author><author><name sortKey="Fields, A" uniqKey="Fields A">A. Fields</name></author><author><name sortKey="Mbawuike, U" uniqKey="Mbawuike U">U. Mbawuike</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Durgan, D J" uniqKey="Durgan D">D. J. Durgan</name></author><author><name sortKey="Trexler, N A" uniqKey="Trexler N">N. A. Trexler</name></author><author><name sortKey="Egbejimi, O" uniqKey="Egbejimi O">O. Egbejimi</name></author><author><name sortKey="Mcelfresh, T A" uniqKey="Mcelfresh T">T. A. McElfresh</name></author><author><name sortKey="Suk, H Y" uniqKey="Suk H">H. Y. Suk</name></author><author><name sortKey="Petterson, L E" uniqKey="Petterson L">L. E. Petterson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Edery, I" uniqKey="Edery I">I. Edery</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Farhat, G N" uniqKey="Farhat G">G. N. Farhat</name></author><author><name sortKey="Cauley, J A" uniqKey="Cauley J">J. A. Cauley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Finck, B N" uniqKey="Finck B">B. N. Finck</name></author><author><name sortKey="Bernal Mizrachi, C" uniqKey="Bernal Mizrachi C">C. Bernal-Mizrachi</name></author><author><name sortKey="Han, D H" uniqKey="Han D">D. H. Han</name></author><author><name sortKey="Coleman, T" uniqKey="Coleman T">T. Coleman</name></author><author><name sortKey="Sambandam, N" uniqKey="Sambandam N">N. Sambandam</name></author><author><name sortKey="Lariviere, L L" uniqKey="Lariviere L">L. L. LaRiviere</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Finck, B N" uniqKey="Finck B">B. N. Finck</name></author><author><name sortKey="Kelly, D P" uniqKey="Kelly D">D. P. Kelly</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Finck, B N" uniqKey="Finck B">B. N. Finck</name></author><author><name sortKey="Lehman, J J" uniqKey="Lehman J">J. J. Lehman</name></author><author><name sortKey="Leone, T C" uniqKey="Leone T">T. C. Leone</name></author><author><name sortKey="Welch, M J" uniqKey="Welch M">M. J. Welch</name></author><author><name sortKey="Bennett, M J" uniqKey="Bennett M">M. J. Bennett</name></author><author><name sortKey="Kovacs, A" uniqKey="Kovacs A">A. Kovacs</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fontaine, C" uniqKey="Fontaine C">C. Fontaine</name></author><author><name sortKey="Dubois, G" uniqKey="Dubois G">G. Dubois</name></author><author><name sortKey="Duguay, Y" uniqKey="Duguay Y">Y. Duguay</name></author><author><name sortKey="Helledie, T" uniqKey="Helledie T">T. Helledie</name></author><author><name sortKey="Vu Dac, N" uniqKey="Vu Dac N">N. Vu-Dac</name></author><author><name sortKey="Gervois, P" uniqKey="Gervois P">P. Gervois</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fontaine, G" uniqKey="Fontaine G">G. Fontaine</name></author><author><name sortKey="Fontaliran, F" uniqKey="Fontaliran F">F. Fontaliran</name></author><author><name sortKey="Hebert, J L" uniqKey="Hebert J">J. L. Hebert</name></author><author><name sortKey="Chemla, D" uniqKey="Chemla D">D. Chemla</name></author><author><name sortKey="Zenati, O" uniqKey="Zenati O">O. Zenati</name></author><author><name sortKey="Lecarpentier, Y" uniqKey="Lecarpentier Y">Y. Lecarpentier</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fressard, V" uniqKey="Fressard V">V. Fressard</name></author><author><name sortKey="Duthoit, G" uniqKey="Duthoit G">G. Duthoit</name></author><author><name sortKey="Donal, E" uniqKey="Donal E">E. Donal</name></author><author><name sortKey="Probst, V" uniqKey="Probst V">V. Probst</name></author><author><name sortKey="Deharo, J C" uniqKey="Deharo J">J.-C. Deharo</name></author><author><name sortKey="Chevalier, P" uniqKey="Chevalier P">P. Chevalier</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Galli, C" uniqKey="Galli C">C. Galli</name></author><author><name sortKey="Piemontese, M" uniqKey="Piemontese M">M. Piemontese</name></author><author><name sortKey="Lumetti, S" uniqKey="Lumetti S">S. Lumetti</name></author><author><name sortKey="Manfredi, E" uniqKey="Manfredi E">E. Manfredi</name></author><author><name sortKey="Macaluso, G M" uniqKey="Macaluso G">G. M. Macaluso</name></author><author><name sortKey="Passeri, G" uniqKey="Passeri G">G. Passeri</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Garcia Gras, E" uniqKey="Garcia Gras E">E. Garcia-Gras</name></author><author><name sortKey="Lombardi, R" uniqKey="Lombardi R">R. Lombardi</name></author><author><name sortKey="Giocondo, M J" uniqKey="Giocondo M">M. J. Giocondo</name></author><author><name sortKey="Willerson, J T" uniqKey="Willerson J">J. T. Willerson</name></author><author><name sortKey="Schneider, M D" uniqKey="Schneider M">M. D. Schneider</name></author><author><name sortKey="Khoury, D S" uniqKey="Khoury D">D. S. Khoury</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gdynia, H J" uniqKey="Gdynia H">H. J. Gdynia</name></author><author><name sortKey="Kurt, A" uniqKey="Kurt A">A. Kurt</name></author><author><name sortKey="Endruhn, S" uniqKey="Endruhn S">S. Endruhn</name></author><author><name sortKey="Ludolph, A C" uniqKey="Ludolph A">A. C. Ludolph</name></author><author><name sortKey="Sperfeld, A D" uniqKey="Sperfeld A">A. D. Sperfeld</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gekakis, N" uniqKey="Gekakis N">N. Gekakis</name></author><author><name sortKey="Staknis, D" uniqKey="Staknis D">D. Staknis</name></author><author><name sortKey="Nguyen, H B" uniqKey="Nguyen H">H. B. Nguyen</name></author><author><name sortKey="Davis, F C" uniqKey="Davis F">F. C. Davis</name></author><author><name sortKey="Wilsbacher, L D" uniqKey="Wilsbacher L">L. D. Wilsbacher</name></author><author><name sortKey="King, D P" uniqKey="King D">D. P. King</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gervois, P" uniqKey="Gervois P">P. Gervois</name></author><author><name sortKey="Chopin Delannoy, S" uniqKey="Chopin Delannoy S">S. Chopin-Delannoy</name></author><author><name sortKey="Fadel, A" uniqKey="Fadel A">A. Fadel</name></author><author><name sortKey="Dubois, G" uniqKey="Dubois G">G. Dubois</name></author><author><name sortKey="Kosykh, V" uniqKey="Kosykh V">V. Kosykh</name></author><author><name sortKey="Fruchart, J C" uniqKey="Fruchart J">J. C. Fruchart</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gibbons, G F" uniqKey="Gibbons G">G. F. Gibbons</name></author><author><name sortKey="Patel, D" uniqKey="Patel D">D. Patel</name></author><author><name sortKey="Wiggins, D" uniqKey="Wiggins D">D. Wiggins</name></author><author><name sortKey="Knight, B L" uniqKey="Knight B">B. L. Knight</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Godin, J D" uniqKey="Godin J">J. D. Godin</name></author><author><name sortKey="Poizat, G" uniqKey="Poizat G">G. Poizat</name></author><author><name sortKey="Hickey, M A" uniqKey="Hickey M">M. A. Hickey</name></author><author><name sortKey="Maschat, F" uniqKey="Maschat F">F. Maschat</name></author><author><name sortKey="Humbert, S" uniqKey="Humbert S">S. Humbert</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Goldbeter, A" uniqKey="Goldbeter A">A. Goldbeter</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Goldbeter, A" uniqKey="Goldbeter A">A. Goldbeter</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Goodwin, B C" uniqKey="Goodwin B">B. C. Goodwin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gould, T D" uniqKey="Gould T">T. D. Gould</name></author><author><name sortKey="Manji, H K" uniqKey="Manji H">H. K. Manji</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Green, C B" uniqKey="Green C">C. B. Green</name></author><author><name sortKey="Douris, N" uniqKey="Douris N">N. Douris</name></author><author><name sortKey="Kojima, S" uniqKey="Kojima S">S. Kojima</name></author><author><name sortKey="Strayer, C A" uniqKey="Strayer C">C. A. Strayer</name></author><author><name sortKey="Fogerty, J" uniqKey="Fogerty J">J. Fogerty</name></author><author><name sortKey="Lourim, D" uniqKey="Lourim D">D. Lourim</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Guo, B" uniqKey="Guo B">B. Guo</name></author><author><name sortKey="Chatterjee, S" uniqKey="Chatterjee S">S. Chatterjee</name></author><author><name sortKey="Li, L" uniqKey="Li L">L. Li</name></author><author><name sortKey="Kim, J M" uniqKey="Kim J">J. M. Kim</name></author><author><name sortKey="Lee, J" uniqKey="Lee J">J. Lee</name></author><author><name sortKey="Yechoor, V K" uniqKey="Yechoor V">V. K. Yechoor</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Haapaniemi, T H" uniqKey="Haapaniemi T">T. H. Haapaniemi</name></author><author><name sortKey="Pursiainen, V" uniqKey="Pursiainen V">V. Pursiainen</name></author><author><name sortKey="Korpelainen, J T" uniqKey="Korpelainen J">J. T. Korpelainen</name></author><author><name sortKey="Huikuri, H V" uniqKey="Huikuri H">H. V. Huikuri</name></author><author><name sortKey="Sotaniemi, K A" uniqKey="Sotaniemi K">K. A. Sotaniemi</name></author><author><name sortKey="Myllyla, V V" uniqKey="Myllyla V">V. V. Myllyla</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hack, N" uniqKey="Hack N">N. Hack</name></author><author><name sortKey="Fayad, S M" uniqKey="Fayad S">S. M. Fayad</name></author><author><name sortKey="Monari, E H" uniqKey="Monari E">E. H. Monari</name></author><author><name sortKey="Akbar, U" uniqKey="Akbar U">U. Akbar</name></author><author><name sortKey="Hardwick, A" uniqKey="Hardwick A">A. Hardwick</name></author><author><name sortKey="Rodriguez, R L" uniqKey="Rodriguez R">R. L. Rodriguez</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Halabi, C M" uniqKey="Halabi C">C. M. Halabi</name></author><author><name sortKey="Beyer, A M" uniqKey="Beyer A">A. M. Beyer</name></author><author><name sortKey="De Lange, W J" uniqKey="De Lange W">W. J. de Lange</name></author><author><name sortKey="Keen, H L" uniqKey="Keen H">H. L. Keen</name></author><author><name sortKey="Baumbach, G L" uniqKey="Baumbach G">G. L. Baumbach</name></author><author><name sortKey="Faraci, F M" uniqKey="Faraci F">F. M. Faraci</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hardin, P E" uniqKey="Hardin P">P. E. Hardin</name></author><author><name sortKey="Hall, J C" uniqKey="Hall J">J. C. Hall</name></author><author><name sortKey="Rosbash, M" uniqKey="Rosbash M">M. Rosbash</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hebert, J L" uniqKey="Hebert J">J. L. Hebert</name></author><author><name sortKey="Chemla, D" uniqKey="Chemla D">D. Chemla</name></author><author><name sortKey="Gerard, O" uniqKey="Gerard O">O. Gerard</name></author><author><name sortKey="Zamani, K" uniqKey="Zamani K">K. Zamani</name></author><author><name sortKey="Quillard, J" uniqKey="Quillard J">J. Quillard</name></author><author><name sortKey="Azarine, A" uniqKey="Azarine A">A. Azarine</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hedgepeth, C M" uniqKey="Hedgepeth C">C. M. Hedgepeth</name></author><author><name sortKey="Conrad, L J" uniqKey="Conrad L">L. J. Conrad</name></author><author><name sortKey="Zhang, J" uniqKey="Zhang J">J. Zhang</name></author><author><name sortKey="Huang, H C" uniqKey="Huang H">H. C. Huang</name></author><author><name sortKey="Lee, V M" uniqKey="Lee V">V. M. Lee</name></author><author><name sortKey="Klein, P S" uniqKey="Klein P">P. S. Klein</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hennekens, C H" uniqKey="Hennekens C">C. H. Hennekens</name></author><author><name sortKey="Hennekens, A R" uniqKey="Hennekens A">A. R. Hennekens</name></author><author><name sortKey="Hollar, D" uniqKey="Hollar D">D. Hollar</name></author><author><name sortKey="Casey, D E" uniqKey="Casey D">D. E. Casey</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Heuberger, J" uniqKey="Heuberger J">J. Heuberger</name></author><author><name sortKey="Birchmeier, W" uniqKey="Birchmeier W">W. Birchmeier</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hineno, T" uniqKey="Hineno T">T. Hineno</name></author><author><name sortKey="Mizobuchi, M" uniqKey="Mizobuchi M">M. Mizobuchi</name></author><author><name sortKey="Hiratani, K" uniqKey="Hiratani K">K. Hiratani</name></author><author><name sortKey="Inami, Y" uniqKey="Inami Y">Y. Inami</name></author><author><name sortKey="Kakimoto, Y" uniqKey="Kakimoto Y">Y. Kakimoto</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hogenesch, J B" uniqKey="Hogenesch J">J. B. Hogenesch</name></author><author><name sortKey="Gu, Y Z" uniqKey="Gu Y">Y. Z. Gu</name></author><author><name sortKey="Jain, S" uniqKey="Jain S">S. Jain</name></author><author><name sortKey="Bradfield, C A" uniqKey="Bradfield C">C. A. Bradfield</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hu, K" uniqKey="Hu K">K. Hu</name></author><author><name sortKey="Ivanov, P" uniqKey="Ivanov P">P. Ivanov</name></author><author><name sortKey="Hilton, M F" uniqKey="Hilton M">M. F. Hilton</name></author><author><name sortKey="Chen, Z" uniqKey="Chen Z">Z. Chen</name></author><author><name sortKey="Ayers, R T" uniqKey="Ayers R">R. T. Ayers</name></author><author><name sortKey="Stanley, H E" uniqKey="Stanley H">H. E. Stanley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Huss, J M" uniqKey="Huss J">J. M. Huss</name></author><author><name sortKey="Levy, F H" uniqKey="Levy F">F. H. Levy</name></author><author><name sortKey="Kelly, D P" uniqKey="Kelly D">D. P. Kelly</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Inestrosa, N C" uniqKey="Inestrosa N">N. C. Inestrosa</name></author><author><name sortKey="Toledo, E M" uniqKey="Toledo E">E. M. Toledo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Inoue, I" uniqKey="Inoue I">I. Inoue</name></author><author><name sortKey="Shinoda, Y" uniqKey="Shinoda Y">Y. Shinoda</name></author><author><name sortKey="Ikeda, M" uniqKey="Ikeda M">M. Ikeda</name></author><author><name sortKey="Hayashi, K" uniqKey="Hayashi K">K. Hayashi</name></author><author><name sortKey="Kanazawa, K" uniqKey="Kanazawa K">K. Kanazawa</name></author><author><name sortKey="Nomura, M" uniqKey="Nomura M">M. Nomura</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ip, W" uniqKey="Ip W">W. Ip</name></author><author><name sortKey="Chiang, Y T" uniqKey="Chiang Y">Y. T. Chiang</name></author><author><name sortKey="Jin, T" uniqKey="Jin T">T. Jin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ivanov, P" uniqKey="Ivanov P">P. Ivanov</name></author><author><name sortKey="Hu, K" uniqKey="Hu K">K. Hu</name></author><author><name sortKey="Hilton, M F" uniqKey="Hilton M">M. F. Hilton</name></author><author><name sortKey="Shea, S A" uniqKey="Shea S">S. A. Shea</name></author><author><name sortKey="Stanley, H E" uniqKey="Stanley H">H. E. Stanley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jadidi, E" uniqKey="Jadidi E">E. Jadidi</name></author><author><name sortKey="Mohammadi, M" uniqKey="Mohammadi M">M. Mohammadi</name></author><author><name sortKey="Moradi, T" uniqKey="Moradi T">T. Moradi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jansson, E A" uniqKey="Jansson E">E. A. Jansson</name></author><author><name sortKey="Are, A" uniqKey="Are A">A. Are</name></author><author><name sortKey="Greicius, G" uniqKey="Greicius G">G. Greicius</name></author><author><name sortKey="Kuo, I C" uniqKey="Kuo I">I. C. Kuo</name></author><author><name sortKey="Kelly, D" uniqKey="Kelly D">D. Kelly</name></author><author><name sortKey="Arulampalam, V" uniqKey="Arulampalam V">V. Arulampalam</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jiang, Q" uniqKey="Jiang Q">Q. Jiang</name></author><author><name sortKey="Heneka, M" uniqKey="Heneka M">M. Heneka</name></author><author><name sortKey="Landreth, G E" uniqKey="Landreth G">G. E. Landreth</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kawai, M" uniqKey="Kawai M">M. Kawai</name></author><author><name sortKey="Green, C B" uniqKey="Green C">C. B. Green</name></author><author><name sortKey="Lecka Czernik, B" uniqKey="Lecka Czernik B">B. Lecka-Czernik</name></author><author><name sortKey="Douris, N" uniqKey="Douris N">N. Douris</name></author><author><name sortKey="Gilbert, M R" uniqKey="Gilbert M">M. R. Gilbert</name></author><author><name sortKey="Kojima, S" uniqKey="Kojima S">S. Kojima</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kelly, D P" uniqKey="Kelly D">D. P. Kelly</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kiaei, M" uniqKey="Kiaei M">M. Kiaei</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kiriazis, H" uniqKey="Kiriazis H">H. Kiriazis</name></author><author><name sortKey="Jennings, N L" uniqKey="Jennings N">N. L. Jennings</name></author><author><name sortKey="Davern, P" uniqKey="Davern P">P. Davern</name></author><author><name sortKey="Lambert, G" uniqKey="Lambert G">G. Lambert</name></author><author><name sortKey="Su, Y" uniqKey="Su Y">Y. Su</name></author><author><name sortKey="Pang, T" uniqKey="Pang T">T. Pang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Klymkowsky, M W" uniqKey="Klymkowsky M">M. W. Klymkowsky</name></author><author><name sortKey="Williams, B O" uniqKey="Williams B">B. O. Williams</name></author><author><name sortKey="Barish, G D" uniqKey="Barish G">G. D. Barish</name></author><author><name sortKey="Varmus, H E" uniqKey="Varmus H">H. E. Varmus</name></author><author><name sortKey="Vourgourakis, Y E" uniqKey="Vourgourakis Y">Y. E. Vourgourakis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kolker, D E" uniqKey="Kolker D">D. E. Kolker</name></author><author><name sortKey="Fukuyama, H" uniqKey="Fukuyama H">H. Fukuyama</name></author><author><name sortKey="Huang, D S" uniqKey="Huang D">D. S. Huang</name></author><author><name sortKey="Takahashi, J S" uniqKey="Takahashi J">J. S. Takahashi</name></author><author><name sortKey="Horton, T H" uniqKey="Horton T">T. H. Horton</name></author><author><name sortKey="Turek, F W" uniqKey="Turek F">F. W. Turek</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Korvala, J" uniqKey="Korvala J">J. Korvala</name></author><author><name sortKey="Juppner, H" uniqKey="Juppner H">H. Juppner</name></author><author><name sortKey="Makitie, O" uniqKey="Makitie O">O. Makitie</name></author><author><name sortKey="Sochett, E" uniqKey="Sochett E">E. Sochett</name></author><author><name sortKey="Schnabel, D" uniqKey="Schnabel D">D. Schnabel</name></author><author><name sortKey="Mora, S" uniqKey="Mora S">S. Mora</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kremer, H P" uniqKey="Kremer H">H. P. Kremer</name></author><author><name sortKey="Roos, R A" uniqKey="Roos R">R. A. Roos</name></author><author><name sortKey="Dingjan, G M" uniqKey="Dingjan G">G. M. Dingjan</name></author><author><name sortKey="Bots, G T" uniqKey="Bots G">G. T. Bots</name></author><author><name sortKey="Bruyn, G W" uniqKey="Bruyn G">G. W. Bruyn</name></author><author><name sortKey="Hofman, M A" uniqKey="Hofman M">M. A. Hofman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Krishnan, J" uniqKey="Krishnan J">J. Krishnan</name></author><author><name sortKey="Suter, M" uniqKey="Suter M">M. Suter</name></author><author><name sortKey="Windak, R" uniqKey="Windak R">R. Windak</name></author><author><name sortKey="Krebs, T" uniqKey="Krebs T">T. Krebs</name></author><author><name sortKey="Felley, A" uniqKey="Felley A">A. Felley</name></author><author><name sortKey="Montessuit, C" uniqKey="Montessuit C">C. Montessuit</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kume, K" uniqKey="Kume K">K. Kume</name></author><author><name sortKey="Zylka, M J" uniqKey="Zylka M">M. J. Zylka</name></author><author><name sortKey="Sriram, S" uniqKey="Sriram S">S. Sriram</name></author><author><name sortKey="Shearman, L P" uniqKey="Shearman L">L. P. Shearman</name></author><author><name sortKey="Weaver, D R" uniqKey="Weaver D">D. R. Weaver</name></author><author><name sortKey="Jin, X" uniqKey="Jin X">X. Jin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lan, M J" uniqKey="Lan M">M. J. Lan</name></author><author><name sortKey="Yuan, P" uniqKey="Yuan P">P. Yuan</name></author><author><name sortKey="Chen, G" uniqKey="Chen G">G. Chen</name></author><author><name sortKey="Manji, H K" uniqKey="Manji H">H. K. Manji</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lecarpentier, Y" uniqKey="Lecarpentier Y">Y. Lecarpentier</name></author><author><name sortKey="Claes, V" uniqKey="Claes V">V. Claes</name></author><author><name sortKey="Hebert, J L" uniqKey="Hebert J">J. L. Hebert</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lee, D K" uniqKey="Lee D">D. K. Lee</name></author><author><name sortKey="Nathan Grantham, R" uniqKey="Nathan Grantham R">R. Nathan Grantham</name></author><author><name sortKey="Trachte, A L" uniqKey="Trachte A">A. L. Trachte</name></author><author><name sortKey="Mannion, J D" uniqKey="Mannion J">J. D. Mannion</name></author><author><name sortKey="Wilson, C L" uniqKey="Wilson C">C. L. Wilson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Leibetseder, V" uniqKey="Leibetseder V">V. Leibetseder</name></author><author><name sortKey="Humpeler, S" uniqKey="Humpeler S">S. Humpeler</name></author><author><name sortKey="Svoboda, M" uniqKey="Svoboda M">M. Svoboda</name></author><author><name sortKey="Schmid, D" uniqKey="Schmid D">D. Schmid</name></author><author><name sortKey="Thalhammer, T" uniqKey="Thalhammer T">T. Thalhammer</name></author><author><name sortKey="Zuckermann, A" uniqKey="Zuckermann A">A. Zuckermann</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lemberger, T" uniqKey="Lemberger T">T. Lemberger</name></author><author><name sortKey="Saladin, R" uniqKey="Saladin R">R. Saladin</name></author><author><name sortKey="Vazquez, M" uniqKey="Vazquez M">M. Vazquez</name></author><author><name sortKey="Assimacopoulos, F" uniqKey="Assimacopoulos F">F. Assimacopoulos</name></author><author><name sortKey="Staels, B" uniqKey="Staels B">B. Staels</name></author><author><name sortKey="Desvergne, B" uniqKey="Desvergne B">B. Desvergne</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lemberger, T" uniqKey="Lemberger T">T. Lemberger</name></author><author><name sortKey="Staels, B" uniqKey="Staels B">B. Staels</name></author><author><name sortKey="Saladin, R" uniqKey="Saladin R">R. Saladin</name></author><author><name sortKey="Desvergne, B" uniqKey="Desvergne B">B. Desvergne</name></author><author><name sortKey="Auwerx, J" uniqKey="Auwerx J">J. Auwerx</name></author><author><name sortKey="Wahli, W" uniqKey="Wahli W">W. Wahli</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="L Episcopo, F" uniqKey="L Episcopo F">F. L'Episcopo</name></author><author><name sortKey="Serapide, M F" uniqKey="Serapide M">M. F. Serapide</name></author><author><name sortKey="Tirolo, C" uniqKey="Tirolo C">C. Tirolo</name></author><author><name sortKey="Testa, N" uniqKey="Testa N">N. Testa</name></author><author><name sortKey="Caniglia, S" uniqKey="Caniglia S">S. Caniglia</name></author><author><name sortKey="Morale, M C" uniqKey="Morale M">M. C. Morale</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="L Episcopo, F" uniqKey="L Episcopo F">F. L'Episcopo</name></author><author><name sortKey="Tirolo, C" uniqKey="Tirolo C">C. Tirolo</name></author><author><name sortKey="Testa, N" uniqKey="Testa N">N. Testa</name></author><author><name sortKey="Caniglia, S" uniqKey="Caniglia S">S. Caniglia</name></author><author><name sortKey="Morale, M C" uniqKey="Morale M">M. C. Morale</name></author><author><name sortKey="Deleidi, M" uniqKey="Deleidi M">M. Deleidi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liang, H" uniqKey="Liang H">H. Liang</name></author><author><name sortKey="Ward, W F" uniqKey="Ward W">W. F. Ward</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, C" uniqKey="Liu C">C. Liu</name></author><author><name sortKey="Li, S" uniqKey="Li S">S. Li</name></author><author><name sortKey="Liu, T" uniqKey="Liu T">T. Liu</name></author><author><name sortKey="Borjigin, J" uniqKey="Borjigin J">J. Borjigin</name></author><author><name sortKey="Lin, J D" uniqKey="Lin J">J. D. Lin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, H" uniqKey="Liu H">H. Liu</name></author><author><name sortKey="Fergusson, M M" uniqKey="Fergusson M">M. M. Fergusson</name></author><author><name sortKey="Castilho, R M" uniqKey="Castilho R">R. M. Castilho</name></author><author><name sortKey="Liu, J" uniqKey="Liu J">J. Liu</name></author><author><name sortKey="Cao, L" uniqKey="Cao L">L. Cao</name></author><author><name sortKey="Chen, J" uniqKey="Chen J">J. Chen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lockyer, P" uniqKey="Lockyer P">P. Lockyer</name></author><author><name sortKey="Schisler, J C" uniqKey="Schisler J">J. C. Schisler</name></author><author><name sortKey="Patterson, C" uniqKey="Patterson C">C. Patterson</name></author><author><name sortKey="Willis, M S" uniqKey="Willis M">M. S. Willis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lo Coco, D" uniqKey="Lo Coco D">D. Lo Coco</name></author><author><name sortKey="Mattaliano, P" uniqKey="Mattaliano P">P. Mattaliano</name></author><author><name sortKey="Spataro, R" uniqKey="Spataro R">R. Spataro</name></author><author><name sortKey="Mattaliano, A" uniqKey="Mattaliano A">A. Mattaliano</name></author><author><name sortKey="La Bella, V" uniqKey="La Bella V">V. La Bella</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lu, D" uniqKey="Lu D">D. Lu</name></author><author><name sortKey="Carson, D A" uniqKey="Carson D">D. A. Carson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Macdonald, B T" uniqKey="Macdonald B">B. T. MacDonald</name></author><author><name sortKey="Tamai, K" uniqKey="Tamai K">K. Tamai</name></author><author><name sortKey="He, X" uniqKey="He X">X. He</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Maeda, O" uniqKey="Maeda O">O. Maeda</name></author><author><name sortKey="Usami, N" uniqKey="Usami N">N. Usami</name></author><author><name sortKey="Kondo, M" uniqKey="Kondo M">M. Kondo</name></author><author><name sortKey="Takahashi, M" uniqKey="Takahashi M">M. Takahashi</name></author><author><name sortKey="Goto, H" uniqKey="Goto H">H. Goto</name></author><author><name sortKey="Shimokata, K" uniqKey="Shimokata K">K. Shimokata</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Marcheva, B" uniqKey="Marcheva B">B. Marcheva</name></author><author><name sortKey="Ramsey, K M" uniqKey="Ramsey K">K. M. Ramsey</name></author><author><name sortKey="Buhr, E D" uniqKey="Buhr E">E. D. Buhr</name></author><author><name sortKey="Kobayashi, Y" uniqKey="Kobayashi Y">Y. Kobayashi</name></author><author><name sortKey="Su, H" uniqKey="Su H">H. Su</name></author><author><name sortKey="Ko, C H" uniqKey="Ko C">C. H. Ko</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Marcus, F I" uniqKey="Marcus F">F. I. Marcus</name></author><author><name sortKey="Fontaine, G H" uniqKey="Fontaine G">G. H. Fontaine</name></author><author><name sortKey="Guiraudon, G" uniqKey="Guiraudon G">G. Guiraudon</name></author><author><name sortKey="Frank, R" uniqKey="Frank R">R. Frank</name></author><author><name sortKey="Laurenceau, J L" uniqKey="Laurenceau J">J. L. Laurenceau</name></author><author><name sortKey="Malergue, C" uniqKey="Malergue C">C. Malergue</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Marmolino, D" uniqKey="Marmolino D">D. Marmolino</name></author><author><name sortKey="Acquaviva, F" uniqKey="Acquaviva F">F. Acquaviva</name></author><author><name sortKey="Pinelli, M" uniqKey="Pinelli M">M. Pinelli</name></author><author><name sortKey="Monticelli, A" uniqKey="Monticelli A">A. Monticelli</name></author><author><name sortKey="Castaldo, I" uniqKey="Castaldo I">I. Castaldo</name></author><author><name sortKey="Filla, A" uniqKey="Filla A">A. Filla</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Maywood, E S" uniqKey="Maywood E">E. S. Maywood</name></author><author><name sortKey="Fraenkel, E" uniqKey="Fraenkel E">E. Fraenkel</name></author><author><name sortKey="Mcallister, C J" uniqKey="Mcallister C">C. J. McAllister</name></author><author><name sortKey="Wood, N" uniqKey="Wood N">N. Wood</name></author><author><name sortKey="Reddy, A B" uniqKey="Reddy A">A. B. Reddy</name></author><author><name sortKey="Hastings, M H" uniqKey="Hastings M">M. H. Hastings</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mcnamara, P" uniqKey="Mcnamara P">P. McNamara</name></author><author><name sortKey="Seo, S B" uniqKey="Seo S">S. B. Seo</name></author><author><name sortKey="Rudic, R D" uniqKey="Rudic R">R. D. Rudic</name></author><author><name sortKey="Sehgal, A" uniqKey="Sehgal A">A. Sehgal</name></author><author><name sortKey="Chakravarti, D" uniqKey="Chakravarti D">D. Chakravarti</name></author><author><name sortKey="Fitzgerald, G A" uniqKey="Fitzgerald G">G. A. FitzGerald</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Meshorer, E" uniqKey="Meshorer E">E. Meshorer</name></author><author><name sortKey="Gruenbaum, Y" uniqKey="Gruenbaum Y">Y. Gruenbaum</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mihm, M J" uniqKey="Mihm M">M. J. Mihm</name></author><author><name sortKey="Amann, D M" uniqKey="Amann D">D. M. Amann</name></author><author><name sortKey="Schanbacher, B L" uniqKey="Schanbacher B">B. L. Schanbacher</name></author><author><name sortKey="Altschuld, R A" uniqKey="Altschuld R">R. A. Altschuld</name></author><author><name sortKey="Bauer, J A" uniqKey="Bauer J">J. A. Bauer</name></author><author><name sortKey="Hoyt, K R" uniqKey="Hoyt K">K. R. Hoyt</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Moldes, M" uniqKey="Moldes M">M. Moldes</name></author><author><name sortKey="Zuo, Y" uniqKey="Zuo Y">Y. Zuo</name></author><author><name sortKey="Morrison, R F" uniqKey="Morrison R">R. F. Morrison</name></author><author><name sortKey="Silva, D" uniqKey="Silva D">D. Silva</name></author><author><name sortKey="Park, B H" uniqKey="Park B">B. H. Park</name></author><author><name sortKey="Liu, J" uniqKey="Liu J">J. Liu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Moon, R T" uniqKey="Moon R">R. T. Moon</name></author><author><name sortKey="Bowerman, B" uniqKey="Bowerman B">B. Bowerman</name></author><author><name sortKey="Boutros, M" uniqKey="Boutros M">M. Boutros</name></author><author><name sortKey="Perrimon, N" uniqKey="Perrimon N">N. Perrimon</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Morin, P J" uniqKey="Morin P">P. J. Morin</name></author><author><name sortKey="Sparks, A B" uniqKey="Sparks A">A. B. Sparks</name></author><author><name sortKey="Korinek, V" uniqKey="Korinek V">V. Korinek</name></author><author><name sortKey="Barker, N" uniqKey="Barker N">N. Barker</name></author><author><name sortKey="Clevers, H" uniqKey="Clevers H">H. Clevers</name></author><author><name sortKey="Vogelstein, B" uniqKey="Vogelstein B">B. Vogelstein</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Musiek, E S" uniqKey="Musiek E">E. S. Musiek</name></author><author><name sortKey="Lim, M M" uniqKey="Lim M">M. M. Lim</name></author><author><name sortKey="Yang, G" uniqKey="Yang G">G. Yang</name></author><author><name sortKey="Bauer, A Q" uniqKey="Bauer A">A. Q. Bauer</name></author><author><name sortKey="Qi, L" uniqKey="Qi L">L. Qi</name></author><author><name sortKey="Lee, Y" uniqKey="Lee Y">Y. Lee</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Naito, A T" uniqKey="Naito A">A. T. Naito</name></author><author><name sortKey="Shiojima, I" uniqKey="Shiojima I">I. Shiojima</name></author><author><name sortKey="Komuro, I" uniqKey="Komuro I">I. Komuro</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Najdi, R" uniqKey="Najdi R">R. Najdi</name></author><author><name sortKey="Holcombe, R F" uniqKey="Holcombe R">R. F. Holcombe</name></author><author><name sortKey="Waterman, M L" uniqKey="Waterman M">M. L. Waterman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Narravula, S" uniqKey="Narravula S">S. Narravula</name></author><author><name sortKey="Colgan, S P" uniqKey="Colgan S">S. P. Colgan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Nicol, C J" uniqKey="Nicol C">C. J. Nicol</name></author><author><name sortKey="Adachi, M" uniqKey="Adachi M">M. Adachi</name></author><author><name sortKey="Akiyama, T E" uniqKey="Akiyama T">T. E. Akiyama</name></author><author><name sortKey="Gonzalez, F J" uniqKey="Gonzalez F">F. J. Gonzalez</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Nonaka, H" uniqKey="Nonaka H">H. Nonaka</name></author><author><name sortKey="Emoto, N" uniqKey="Emoto N">N. Emoto</name></author><author><name sortKey="Ikeda, K" uniqKey="Ikeda K">K. Ikeda</name></author><author><name sortKey="Fukuya, H" uniqKey="Fukuya H">H. Fukuya</name></author><author><name sortKey="Rohman, M S" uniqKey="Rohman M">M. S. Rohman</name></author><author><name sortKey="Raharjo, S B" uniqKey="Raharjo S">S. B. Raharjo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Oishi, K" uniqKey="Oishi K">K. Oishi</name></author><author><name sortKey="Shirai, H" uniqKey="Shirai H">H. Shirai</name></author><author><name sortKey="Ishida, N" uniqKey="Ishida N">N. Ishida</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Oishi, K" uniqKey="Oishi K">K. Oishi</name></author><author><name sortKey="Shirai, H" uniqKey="Shirai H">H. Shirai</name></author><author><name sortKey="Ishida, N" uniqKey="Ishida N">N. Ishida</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="O Neal, W T" uniqKey="O Neal W">W. T. O'Neal</name></author><author><name sortKey="Griffin, W F" uniqKey="Griffin W">W. F. Griffin</name></author><author><name sortKey="Dries Devlin, J L" uniqKey="Dries Devlin J">J. L. Dries-Devlin</name></author><author><name sortKey="Kent, S D" uniqKey="Kent S">S. D. Kent</name></author><author><name sortKey="Chen, J" uniqKey="Chen J">J. Chen</name></author><author><name sortKey="Willis, M S" uniqKey="Willis M">M. S. Willis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pallier, P N" uniqKey="Pallier P">P. N. Pallier</name></author><author><name sortKey="Morton, A J" uniqKey="Morton A">A. J. Morton</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Paschos, G K" uniqKey="Paschos G">G. K. Paschos</name></author><author><name sortKey="Ibrahim, S" uniqKey="Ibrahim S">S. Ibrahim</name></author><author><name sortKey="Song, W L" uniqKey="Song W">W. L. Song</name></author><author><name sortKey="Kunieda, T" uniqKey="Kunieda T">T. Kunieda</name></author><author><name sortKey="Grant, G" uniqKey="Grant G">G. Grant</name></author><author><name sortKey="Reyes, T M" uniqKey="Reyes T">T. M. Reyes</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Patacchioli, F R" uniqKey="Patacchioli F">F. R. Patacchioli</name></author><author><name sortKey="Monnazzi, P" uniqKey="Monnazzi P">P. Monnazzi</name></author><author><name sortKey="Scontrini, A" uniqKey="Scontrini A">A. Scontrini</name></author><author><name sortKey="Tremante, E" uniqKey="Tremante E">E. Tremante</name></author><author><name sortKey="Caridi, I" uniqKey="Caridi I">I. Caridi</name></author><author><name sortKey="Brunetti, E" uniqKey="Brunetti E">E. Brunetti</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Patel, D D" uniqKey="Patel D">D. D. Patel</name></author><author><name sortKey="Knight, B L" uniqKey="Knight B">B. L. Knight</name></author><author><name sortKey="Wiggins, D" uniqKey="Wiggins D">D. Wiggins</name></author><author><name sortKey="Humphreys, S M" uniqKey="Humphreys S">S. M. Humphreys</name></author><author><name sortKey="Gibbons, G F" uniqKey="Gibbons G">G. F. Gibbons</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pinto, C" uniqKey="Pinto C">C. Pinto</name></author><author><name sortKey="Cardenas, P" uniqKey="Cardenas P">P. Cardenas</name></author><author><name sortKey="Osses, N" uniqKey="Osses N">N. Osses</name></author><author><name sortKey="Henriquez, J P" uniqKey="Henriquez J">J. P. Henriquez</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Postuma, R B" uniqKey="Postuma R">R. B. Postuma</name></author><author><name sortKey="Montplaisir, J" uniqKey="Montplaisir J">J. Montplaisir</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Preitner, N" uniqKey="Preitner N">N. Preitner</name></author><author><name sortKey="Damiola, F" uniqKey="Damiola F">F. Damiola</name></author><author><name sortKey="Lopez Molina, L" uniqKey="Lopez Molina L">L. Lopez-Molina</name></author><author><name sortKey="Zakany, J" uniqKey="Zakany J">J. Zakany</name></author><author><name sortKey="Duboule, D" uniqKey="Duboule D">D. Duboule</name></author><author><name sortKey="Albrecht, U" uniqKey="Albrecht U">U. Albrecht</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Prigogine, I" uniqKey="Prigogine I">I. Prigogine</name></author><author><name sortKey="Nicolis, G" uniqKey="Nicolis G">G. Nicolis</name></author><author><name sortKey="Babloyantz, A" uniqKey="Babloyantz A">A. Babloyantz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rawadi, G" uniqKey="Rawadi G">G. Rawadi</name></author><author><name sortKey="Roman Roman, S" uniqKey="Roman Roman S">S. Roman-Roman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Razeghi, P" uniqKey="Razeghi P">P. Razeghi</name></author><author><name sortKey="Young, M E" uniqKey="Young M">M. E. Young</name></author><author><name sortKey="Abbasi, S" uniqKey="Abbasi S">S. Abbasi</name></author><author><name sortKey="Taegtmeyer, H" uniqKey="Taegtmeyer H">H. Taegtmeyer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Reppert, S M" uniqKey="Reppert S">S. M. Reppert</name></author><author><name sortKey="Weaver, D R" uniqKey="Weaver D">D. R. Weaver</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Reppert, S M" uniqKey="Reppert S">S. M. Reppert</name></author><author><name sortKey="Weaver, D R" uniqKey="Weaver D">D. R. Weaver</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Richardson, P" uniqKey="Richardson P">P. Richardson</name></author><author><name sortKey="Mckenna, W" uniqKey="Mckenna W">W. McKenna</name></author><author><name sortKey="Bristow, M" uniqKey="Bristow M">M. Bristow</name></author><author><name sortKey="Maisch, B" uniqKey="Maisch B">B. Maisch</name></author><author><name sortKey="Mautner, B" uniqKey="Mautner B">B. Mautner</name></author><author><name sortKey="O Connell, J" uniqKey="O Connell J">J. O'Connell</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ross, O A" uniqKey="Ross O">O. A. Ross</name></author><author><name sortKey="Rutherford, N J" uniqKey="Rutherford N">N. J. Rutherford</name></author><author><name sortKey="Baker, M" uniqKey="Baker M">M. Baker</name></author><author><name sortKey="Soto Ortolaza, A I" uniqKey="Soto Ortolaza A">A. I. Soto-Ortolaza</name></author><author><name sortKey="Carrasquillo, M M" uniqKey="Carrasquillo M">M. M. Carrasquillo</name></author><author><name sortKey="Dejesus Hernandez, M" uniqKey="Dejesus Hernandez M">M. DeJesus-Hernandez</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ross, S E" uniqKey="Ross S">S. E. Ross</name></author><author><name sortKey="Hemati, N" uniqKey="Hemati N">N. Hemati</name></author><author><name sortKey="Longo, K A" uniqKey="Longo K">K. A. Longo</name></author><author><name sortKey="Bennett, C N" uniqKey="Bennett C">C. N. Bennett</name></author><author><name sortKey="Lucas, P C" uniqKey="Lucas P">P. C. Lucas</name></author><author><name sortKey="Erickson, R L" uniqKey="Erickson R">R. L. Erickson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rudic, R D" uniqKey="Rudic R">R. D. Rudic</name></author><author><name sortKey="Fulton, D J" uniqKey="Fulton D">D. J. Fulton</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ryan, M J" uniqKey="Ryan M">M. J. Ryan</name></author><author><name sortKey="Didion, S P" uniqKey="Didion S">S. P. Didion</name></author><author><name sortKey="Mathur, S" uniqKey="Mathur S">S. Mathur</name></author><author><name sortKey="Faraci, F M" uniqKey="Faraci F">F. M. Faraci</name></author><author><name sortKey="Sigmund, C D" uniqKey="Sigmund C">C. D. Sigmund</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sakai, T" uniqKey="Sakai T">T. Sakai</name></author><author><name sortKey="Tamura, T" uniqKey="Tamura T">T. Tamura</name></author><author><name sortKey="Kitamoto, T" uniqKey="Kitamoto T">T. Kitamoto</name></author><author><name sortKey="Kidokoro, Y" uniqKey="Kidokoro Y">Y. Kidokoro</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sarraf, P" uniqKey="Sarraf P">P. Sarraf</name></author><author><name sortKey="Mueller, E" uniqKey="Mueller E">E. Mueller</name></author><author><name sortKey="Smith, W M" uniqKey="Smith W">W. M. Smith</name></author><author><name sortKey="Wright, H M" uniqKey="Wright H">H. M. Wright</name></author><author><name sortKey="Kum, J B" uniqKey="Kum J">J. B. Kum</name></author><author><name sortKey="Aaltonen, L A" uniqKey="Aaltonen L">L. A. Aaltonen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Savvidis, C" uniqKey="Savvidis C">C. Savvidis</name></author><author><name sortKey="Koutsilieris, M" uniqKey="Koutsilieris M">M. Koutsilieris</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schibler, U" uniqKey="Schibler U">U. Schibler</name></author><author><name sortKey="Sassone Corsi, P" uniqKey="Sassone Corsi P">P. Sassone-Corsi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schintu, N" uniqKey="Schintu N">N. Schintu</name></author><author><name sortKey="Frau, L" uniqKey="Frau L">L. Frau</name></author><author><name sortKey="Ibba, M" uniqKey="Ibba M">M. Ibba</name></author><author><name sortKey="Caboni, P" uniqKey="Caboni P">P. Caboni</name></author><author><name sortKey="Garau, A" uniqKey="Garau A">A. Garau</name></author><author><name sortKey="Carboni, E" uniqKey="Carboni E">E. Carboni</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schroeder, A M" uniqKey="Schroeder A">A. M. Schroeder</name></author><author><name sortKey="Loh, D H" uniqKey="Loh D">D. H. Loh</name></author><author><name sortKey="Jordan, M C" uniqKey="Jordan M">M. C. Jordan</name></author><author><name sortKey="Roos, K P" uniqKey="Roos K">K. P. Roos</name></author><author><name sortKey="Colwell, C S" uniqKey="Colwell C">C. S. Colwell</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sen Chowdhry, S" uniqKey="Sen Chowdhry S">S. Sen-Chowdhry</name></author><author><name sortKey="Syrris, P" uniqKey="Syrris P">P. Syrris</name></author><author><name sortKey="Mckenna, W J" uniqKey="Mckenna W">W. J. McKenna</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shirai, H" uniqKey="Shirai H">H. Shirai</name></author><author><name sortKey="Oishi, K" uniqKey="Oishi K">K. Oishi</name></author><author><name sortKey="Kudo, T" uniqKey="Kudo T">T. Kudo</name></author><author><name sortKey="Shibata, S" uniqKey="Shibata S">S. Shibata</name></author><author><name sortKey="Ishida, N" uniqKey="Ishida N">N. Ishida</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Singh, K K" uniqKey="Singh K">K. K. Singh</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sinha, D" uniqKey="Sinha D">D. Sinha</name></author><author><name sortKey="Wang, Z" uniqKey="Wang Z">Z. Wang</name></author><author><name sortKey="Ruchalski, K L" uniqKey="Ruchalski K">K. L. Ruchalski</name></author><author><name sortKey="Levine, J S" uniqKey="Levine J">J. S. Levine</name></author><author><name sortKey="Krishnan, S" uniqKey="Krishnan S">S. Krishnan</name></author><author><name sortKey="Lieberthal, W" uniqKey="Lieberthal W">W. Lieberthal</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stampfer, M J" uniqKey="Stampfer M">M. J. Stampfer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Storch, K F" uniqKey="Storch K">K. F. Storch</name></author><author><name sortKey="Lipan, O" uniqKey="Lipan O">O. Lipan</name></author><author><name sortKey="Leykin, I" uniqKey="Leykin I">I. Leykin</name></author><author><name sortKey="Viswanathan, N" uniqKey="Viswanathan N">N. Viswanathan</name></author><author><name sortKey="Davis, F C" uniqKey="Davis F">F. C. Davis</name></author><author><name sortKey="Wong, W H" uniqKey="Wong W">W. H. Wong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sugawara, A" uniqKey="Sugawara A">A. Sugawara</name></author><author><name sortKey="Uruno, A" uniqKey="Uruno A">A. Uruno</name></author><author><name sortKey="Kudo, M" uniqKey="Kudo M">M. Kudo</name></author><author><name sortKey="Matsuda, K" uniqKey="Matsuda K">K. Matsuda</name></author><author><name sortKey="Yang, C W" uniqKey="Yang C">C. W. Yang</name></author><author><name sortKey="Ito, S" uniqKey="Ito S">S. Ito</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Swanson, C R" uniqKey="Swanson C">C. R. Swanson</name></author><author><name sortKey="Joers, V" uniqKey="Joers V">V. Joers</name></author><author><name sortKey="Bondarenko, V" uniqKey="Bondarenko V">V. Bondarenko</name></author><author><name sortKey="Brunner, K" uniqKey="Brunner K">K. Brunner</name></author><author><name sortKey="Simmons, H A" uniqKey="Simmons H">H. A. Simmons</name></author><author><name sortKey="Ziegler, T E" uniqKey="Ziegler T">T. E. Ziegler</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Swartz, H A" uniqKey="Swartz H">H. A. Swartz</name></author><author><name sortKey="Fagiolini, A" uniqKey="Fagiolini A">A. Fagiolini</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Takada, I" uniqKey="Takada I">I. Takada</name></author><author><name sortKey="Kouzmenko, A P" uniqKey="Kouzmenko A">A. P. Kouzmenko</name></author><author><name sortKey="Kato, S" uniqKey="Kato S">S. Kato</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Takeda, N" uniqKey="Takeda N">N. Takeda</name></author><author><name sortKey="Maemura, K" uniqKey="Maemura K">K. Maemura</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Takeda, N" uniqKey="Takeda N">N. Takeda</name></author><author><name sortKey="Maemura, K" uniqKey="Maemura K">K. Maemura</name></author><author><name sortKey="Horie, S" uniqKey="Horie S">S. Horie</name></author><author><name sortKey="Oishi, K" uniqKey="Oishi K">K. Oishi</name></author><author><name sortKey="Imai, Y" uniqKey="Imai Y">Y. Imai</name></author><author><name sortKey="Harada, T" uniqKey="Harada T">T. Harada</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tougas, G" uniqKey="Tougas G">G. Tougas</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ueda, H R" uniqKey="Ueda H">H. R. Ueda</name></author><author><name sortKey="Chen, W" uniqKey="Chen W">W. Chen</name></author><author><name sortKey="Adachi, A" uniqKey="Adachi A">A. Adachi</name></author><author><name sortKey="Wakamatsu, H" uniqKey="Wakamatsu H">H. Wakamatsu</name></author><author><name sortKey="Hayashi, S" uniqKey="Hayashi S">S. Hayashi</name></author><author><name sortKey="Takasugi, T" uniqKey="Takasugi T">T. Takasugi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Valvezan, A J" uniqKey="Valvezan A">A. J. Valvezan</name></author><author><name sortKey="Klein, P S" uniqKey="Klein P">P. S. Klein</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Viola, A U" uniqKey="Viola A">A. U. Viola</name></author><author><name sortKey="James, L M" uniqKey="James L">L. M. James</name></author><author><name sortKey="Archer, S N" uniqKey="Archer S">S. N. Archer</name></author><author><name sortKey="Dijk, D J" uniqKey="Dijk D">D. J. Dijk</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Virag, J A" uniqKey="Virag J">J. A. Virag</name></author><author><name sortKey="Anderson, E J" uniqKey="Anderson E">E. J. Anderson</name></author><author><name sortKey="Kent, S D" uniqKey="Kent S">S. D. Kent</name></author><author><name sortKey="Blanton, H D" uniqKey="Blanton H">H. D. Blanton</name></author><author><name sortKey="Johnson, T L" uniqKey="Johnson T">T. L. Johnson</name></author><author><name sortKey="Moukdar, F" uniqKey="Moukdar F">F. Moukdar</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Walker, F O" uniqKey="Walker F">F. O. Walker</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wan, W" uniqKey="Wan W">W. Wan</name></author><author><name sortKey="Xia, S" uniqKey="Xia S">S. Xia</name></author><author><name sortKey="Kalionis, B" uniqKey="Kalionis B">B. Kalionis</name></author><author><name sortKey="Liu, L" uniqKey="Liu L">L. Liu</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y. Li</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wan, Y" uniqKey="Wan Y">Y. Wan</name></author><author><name sortKey="Chong, L W" uniqKey="Chong L">L. W. Chong</name></author><author><name sortKey="Evans, R M" uniqKey="Evans R">R. M. Evans</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, J" uniqKey="Wang J">J. Wang</name></author><author><name sortKey="Yin, L" uniqKey="Yin L">L. Yin</name></author><author><name sortKey="Lazar, M A" uniqKey="Lazar M">M. A. Lazar</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, N" uniqKey="Wang N">N. Wang</name></author><author><name sortKey="Yang, G" uniqKey="Yang G">G. Yang</name></author><author><name sortKey="Jia, Z" uniqKey="Jia Z">Z. Jia</name></author><author><name sortKey="Zhang, H" uniqKey="Zhang H">H. Zhang</name></author><author><name sortKey="Aoyagi, T" uniqKey="Aoyagi T">T. Aoyagi</name></author><author><name sortKey="Soodvilai, S" uniqKey="Soodvilai S">S. Soodvilai</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Xiao, Y" uniqKey="Xiao Y">Y. Xiao</name></author><author><name sortKey="Mou, Y" uniqKey="Mou Y">Y. Mou</name></author><author><name sortKey="Zhao, Y" uniqKey="Zhao Y">Y. Zhao</name></author><author><name sortKey="Blankesteijn, W M" uniqKey="Blankesteijn W">W. M. Blankesteijn</name></author><author><name sortKey="Hall, J L" uniqKey="Hall J">J. L. Hall</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Weaver, D R" uniqKey="Weaver D">D. R. Weaver</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Woon, P Y" uniqKey="Woon P">P. Y. Woon</name></author><author><name sortKey="Kaisaki, P J" uniqKey="Kaisaki P">P. J. Kaisaki</name></author><author><name sortKey="Braganca, J" uniqKey="Braganca J">J. Braganca</name></author><author><name sortKey="Bihoreau, M T" uniqKey="Bihoreau M">M. T. Bihoreau</name></author><author><name sortKey="Levy, J C" uniqKey="Levy J">J. C. Levy</name></author><author><name sortKey="Farrall, M" uniqKey="Farrall M">M. Farrall</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wu, X" uniqKey="Wu X">X. Wu</name></author><author><name sortKey="Liu, Z" uniqKey="Liu Z">Z. Liu</name></author><author><name sortKey="Shi, G" uniqKey="Shi G">G. Shi</name></author><author><name sortKey="Xing, L" uniqKey="Xing L">L. Xing</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Gu, X" uniqKey="Gu X">X. Gu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wulff, K" uniqKey="Wulff K">K. Wulff</name></author><author><name sortKey="Dijk, D J" uniqKey="Dijk D">D. J. Dijk</name></author><author><name sortKey="Middleton, B" uniqKey="Middleton B">B. Middleton</name></author><author><name sortKey="Foster, R G" uniqKey="Foster R">R. G. Foster</name></author><author><name sortKey="Joyce, E M" uniqKey="Joyce E">E. M. Joyce</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, G" uniqKey="Yang G">G. Yang</name></author><author><name sortKey="Jia, Z" uniqKey="Jia Z">Z. Jia</name></author><author><name sortKey="Aoyagi, T" uniqKey="Aoyagi T">T. Aoyagi</name></author><author><name sortKey="Mcclain, D" uniqKey="Mcclain D">D. McClain</name></author><author><name sortKey="Mortensen, R M" uniqKey="Mortensen R">R. M. Mortensen</name></author><author><name sortKey="Yang, T" uniqKey="Yang T">T. Yang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, T" uniqKey="Yang T">T. Yang</name></author><author><name sortKey="Aoyagi, T" uniqKey="Aoyagi T">T. Aoyagi</name></author><author><name sortKey="Dowtown, M" uniqKey="Dowtown M">M. Dowtown</name></author><author><name sortKey="Liu, M" uniqKey="Liu M">M. Liu</name></author><author><name sortKey="Whitehead, K" uniqKey="Whitehead K">K. Whitehead</name></author><author><name sortKey="Jia, Z" uniqKey="Jia Z">Z. Jia</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, X" uniqKey="Yang X">X. Yang</name></author><author><name sortKey="Downes, M" uniqKey="Downes M">M. Downes</name></author><author><name sortKey="Yu, R T" uniqKey="Yu R">R. T. Yu</name></author><author><name sortKey="Bookout, A L" uniqKey="Bookout A">A. L. Bookout</name></author><author><name sortKey="He, W" uniqKey="He W">W. He</name></author><author><name sortKey="Straume, M" uniqKey="Straume M">M. Straume</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, Y" uniqKey="Yang Y">Y. Yang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yin, L" uniqKey="Yin L">L. Yin</name></author><author><name sortKey="Wang, J" uniqKey="Wang J">J. Wang</name></author><author><name sortKey="Klein, P S" uniqKey="Klein P">P. S. Klein</name></author><author><name sortKey="Lazar, M A" uniqKey="Lazar M">M. A. Lazar</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Young, M E" uniqKey="Young M">M. E. Young</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Young, M E" uniqKey="Young M">M. E. Young</name></author><author><name sortKey="Laws, F A" uniqKey="Laws F">F. A. Laws</name></author><author><name sortKey="Goodwin, G W" uniqKey="Goodwin G">G. W. Goodwin</name></author><author><name sortKey="Taegtmeyer, H" uniqKey="Taegtmeyer H">H. Taegtmeyer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Young, M E" uniqKey="Young M">M. E. Young</name></author><author><name sortKey="Razeghi, P" uniqKey="Razeghi P">P. Razeghi</name></author><author><name sortKey="Cedars, A M" uniqKey="Cedars A">A. M. Cedars</name></author><author><name sortKey="Guthrie, P H" uniqKey="Guthrie P">P. H. Guthrie</name></author><author><name sortKey="Taegtmeyer, H" uniqKey="Taegtmeyer H">H. Taegtmeyer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Young, M E" uniqKey="Young M">M. E. Young</name></author><author><name sortKey="Razeghi, P" uniqKey="Razeghi P">P. Razeghi</name></author><author><name sortKey="Taegtmeyer, H" uniqKey="Taegtmeyer H">H. Taegtmeyer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Young, M E" uniqKey="Young M">M. E. Young</name></author><author><name sortKey="Wilson, C R" uniqKey="Wilson C">C. R. Wilson</name></author><author><name sortKey="Razeghi, P" uniqKey="Razeghi P">P. Razeghi</name></author><author><name sortKey="Guthrie, P H" uniqKey="Guthrie P">P. H. Guthrie</name></author><author><name sortKey="Taegtmeyer, H" uniqKey="Taegtmeyer H">H. Taegtmeyer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Young, M W" uniqKey="Young M">M. W. Young</name></author><author><name sortKey="Kay, S A" uniqKey="Kay S">S. A. Kay</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yu, Y" uniqKey="Yu Y">Y. Yu</name></author><author><name sortKey="Zhang, Z H" uniqKey="Zhang Z">Z. H. Zhang</name></author><author><name sortKey="Wei, S G" uniqKey="Wei S">S. G. Wei</name></author><author><name sortKey="Weiss, R M" uniqKey="Weiss R">R. M. Weiss</name></author><author><name sortKey="Felder, R B" uniqKey="Felder R">R. B. Felder</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yuan, S" uniqKey="Yuan S">S. Yuan</name></author><author><name sortKey="Shi, Y" uniqKey="Shi Y">Y. Shi</name></author><author><name sortKey="Tang, S J" uniqKey="Tang S">S. J. Tang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yuhara, H" uniqKey="Yuhara H">H. Yuhara</name></author><author><name sortKey="Steinmaus, C" uniqKey="Steinmaus C">C. Steinmaus</name></author><author><name sortKey="Cohen, S E" uniqKey="Cohen S">S. E. Cohen</name></author><author><name sortKey="Corley, D A" uniqKey="Corley D">D. A. Corley</name></author><author><name sortKey="Tei, Y" uniqKey="Tei Y">Y. Tei</name></author><author><name sortKey="Buffler, P A" uniqKey="Buffler P">P. A. Buffler</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhu, L" uniqKey="Zhu L">L. Zhu</name></author><author><name sortKey="Wang, Q" uniqKey="Wang Q">Q. Wang</name></author><author><name sortKey="Zhang, L" uniqKey="Zhang L">L. Zhang</name></author><author><name sortKey="Fang, Z" uniqKey="Fang Z">Z. Fang</name></author><author><name sortKey="Zhao, F" uniqKey="Zhao F">F. Zhao</name></author><author><name sortKey="Lv, Z" uniqKey="Lv Z">Z. Lv</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhurinsky, J" uniqKey="Zhurinsky J">J. Zhurinsky</name></author><author><name sortKey="Shtutman, M" uniqKey="Shtutman M">M. Shtutman</name></author><author><name sortKey="Ben Ze Ev, A" uniqKey="Ben Ze Ev A">A. Ben-Ze'ev</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zylka, M J" uniqKey="Zylka M">M. J. Zylka</name></author><author><name sortKey="Shearman, L P" uniqKey="Shearman L">L. P. Shearman</name></author><author><name sortKey="Weaver, D R" uniqKey="Weaver D">D. R. Weaver</name></author><author><name sortKey="Reppert, S M" uniqKey="Reppert S">S. M. Reppert</name></author></analytic></biblStruct></listBibl></div1></back></TEI><pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Physiol</journal-id><journal-id journal-id-type="iso-abbrev">Front Physiol</journal-id><journal-id journal-id-type="publisher-id">Front. Physiol.</journal-id><journal-title-group><journal-title>Frontiers in Physiology</journal-title></journal-title-group><issn pub-type="epub">1664-042X</issn><publisher><publisher-name>Frontiers Media S.A.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">25414671</article-id><article-id pub-id-type="pmc">4220097</article-id><article-id pub-id-type="doi">10.3389/fphys.2014.00429</article-id><article-categories><subj-group subj-group-type="heading"><subject>Physiology</subject><subj-group><subject>Review Article</subject></subj-group></subj-group></article-categories><title-group><article-title>Circadian rhythms, Wnt/beta-catenin pathway and PPAR alpha/gamma profiles in diseases with primary or secondary cardiac dysfunction</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Lecarpentier</surname><given-names>Yves</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="author-notes" rid="fn001"><sup>*</sup></xref><uri xlink:type="simple" xlink:href="http://community.frontiersin.org/people/u/139386"></uri></contrib><contrib contrib-type="author"><name><surname>Claes</surname><given-names>Victor</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Duthoit</surname><given-names>Guillaume</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Hébert</surname><given-names>Jean-Louis</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref></contrib></contrib-group><aff id="aff1"><sup>1</sup><institution>Centre de Recherche Clinique, Centre Hospitalier Régional de Meaux</institution><country>Meaux, France</country></aff><aff id="aff2"><sup>2</sup><institution>Department of Pharmaceutical Sciences, University of Antwerp</institution><country>Wilrijk, Belgium</country></aff><aff id="aff3"><sup>3</sup><institution>Institut de Cardiologie, Hôpital de la Pitié-Salpêtière</institution><country>Paris, France</country></aff><author-notes><fn fn-type="edited-by"><p>Edited by: Jitka A. I. Virag, Brody School of Medicine, USA</p></fn><fn fn-type="edited-by"><p>Reviewed by: James Todd Pearson, Monash University, Australia; Ming Gong, University of Kentucky, USA</p></fn><corresp id="fn001">*Correspondence: Yves Lecarpentier, Centre de Recherche Clinique, Hôpital de Meaux, 6-8 rue Saint Fiacre, 77100 Meaux, France e-mail: <email xlink:type="simple">yves.c.lecarpentier@gmail.com</email></corresp><fn fn-type="other" id="fn002"><p>This article was submitted to Integrative Physiology, a section of the journal Frontiers in Physiology.</p></fn></author-notes><pub-date pub-type="epub"><day>04</day><month>11</month><year>2014</year></pub-date><pub-date pub-type="collection"><year>2014</year></pub-date><volume>5</volume><elocation-id>429</elocation-id><history><date date-type="received"><day>16</day><month>7</month><year>2014</year></date><date date-type="accepted"><day>15</day><month>10</month><year>2014</year></date></history><permissions><copyright-statement>Copyright © 2014 Lecarpentier, Claes, Duthoit and Hébert.</copyright-statement><copyright-year>2014</copyright-year><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p></license></permissions><abstract><p>Circadian clock mechanisms are far-from-equilibrium dissipative structures. Peroxisome proliferator-activated receptors (PPAR alpha, beta/delta, and gamma) play a key role in metabolic regulatory processes, particularly in heart muscle. Links between circadian rhythms (CRs) and PPARs have been established. Mammalian CRs involve at least two critical transcription factors, CLOCK and BMAL1 (Gekakis et al., <xref rid="B51" ref-type="bibr">1998</xref>; Hogenesch et al., <xref rid="B70" ref-type="bibr">1998</xref>). PPAR gamma plays a major role in both glucose and lipid metabolisms and presents circadian properties which coordinate the interplay between metabolism and CRs. PPAR gamma is a major component of the vascular clock. Vascular PPAR gamma is a peripheral regulator of cardiovascular rhythms controlling circadian variations in blood pressure and heart rate through BMAL1. We focused our review on diseases with abnormalities of CRs and with primary or secondary cardiac dysfunction. Moreover, these diseases presented changes in the Wnt/beta-catenin pathway and PPARs, according to two opposed profiles. Profile 1 was defined as follows: inactivation of the Wnt/beta-catenin pathway with increased expression of PPAR gamma. Profile 2 was defined as follows: activation of the Wnt/beta-catenin pathway with decreased expression of PPAR gamma. A typical profile 1 disease is arrhythmogenic right ventricular cardiomyopathy, a genetic cardiac disease which presents mutations of the desmosomal proteins and is mainly characterized by fatty acid accumulation in adult cardiomyocytes mainly in the right ventricle. The link between PPAR gamma dysfunction and desmosomal genetic mutations occurs via inactivation of the Wnt/beta-catenin pathway presenting oscillatory properties. A typical profile 2 disease is type 2 diabetes, with activation of the Wnt/beta-catenin pathway and decreased expression of PPAR gamma. CRs abnormalities are present in numerous pathologies such as cardiovascular diseases, sympathetic/parasympathetic dysfunction, hypertension, diabetes, neurodegenerative diseases, cancer which are often closely inter-related.</p></abstract><kwd-group><kwd>circadian rhythms</kwd><kwd>Wnt/beta-catenin</kwd><kwd>PPAR</kwd><kwd>diabetes</kwd><kwd>hypertension</kwd><kwd>myocardial ischemia</kwd><kwd>neurodegenerative diseases</kwd><kwd>colon cancer</kwd></kwd-group><counts><fig-count count="2"></fig-count><table-count count="0"></table-count><equation-count count="0"></equation-count><ref-count count="191"></ref-count><page-count count="16"></page-count><word-count count="15356"></word-count></counts></article-meta></front><body><sec sec-type="intro" id="s1"><title>Introduction</title><p>CRs are biological temporal processes that display endogenous, entrainable free-running periods that last approximately 24 h. They are driven by molecular internal clocks which can be reset by environmental light-dark cycles. Circadian clocks are transcriptionally based molecular mechanisms which comprise feedback loops (Edery, <xref rid="B40" ref-type="bibr">2000</xref>). The molecular basis of CRs have first been clarified in Drosophila and Neurospora, then in cyanobacteria, plants, and mammals (Reppert and Weaver, <xref rid="B136" ref-type="bibr">2002</xref>). All living organisms adjust their physiology and behavior to the 24-h day-night cycle under the governance of circadian clocks. Circadian clocks may provide a selective advantage of anticipation, thus allowing organisms to respond efficiently to various stimuli at the appropriate time. In mammals, sleep-awake and feeding patterns, hormone secretion, heart rate, blood pressure, energy metabolism, and body temperature exhibit CRs. Their disruptions may have deleterious effects. People submitted to shift working, frequent transmeridian air flight, exposure to artificial light exhibit a particularly high incidence of metabolic syndrome and obesity. CR dysfunctions in blood pressure and heart rate, which are both partly regulated by PPAR gamma are involved in arrhythmias which may lead to sudden cardiac death, myocardial infarction or stroke, often occurring at the early morning during the surge in blood pressure. CRs are dissipative structures due to a negative feedback produced by a protein on the expression of its own gene (Goodwin, <xref rid="B57" ref-type="bibr">1965</xref>; Hardin et al., <xref rid="B64" ref-type="bibr">1990</xref>). They operate far-from- equilibrium and generate order spontaneously by exchanging energy with their external environment (Prigogine et al., <xref rid="B132" ref-type="bibr">1974</xref>; Goldbeter, <xref rid="B55" ref-type="bibr">2002</xref>; Lecarpentier et al., <xref rid="B91" ref-type="bibr">2010</xref>).</p></sec><sec><title>The regulatory sites of circadian rhythms</title><p>The master regulator site of CRs is the suprachiasmatic nucleus (SCN) inside the hypothalamus in which core clock genes are rhythmically expressed (Weaver, <xref rid="B171" ref-type="bibr">1998</xref>). In addition to this central clock, each organ has its own biological clock system, termed peripheral clock. The SCN and most peripheral tissues such as heart, blood vessels, skeletal muscles, kidneys, liver, and fat, govern numerous functions that are synchronized with the sleep-awake cycle (Zylka et al., <xref rid="B191" ref-type="bibr">1998</xref>). In the cardiovascular system, circadian clocks have been described within numerous mammalian cells, such as cardiomyocytes, vascular smooth muscle cells, endothelial cells, and fibroblasts (McNamara et al., <xref rid="B110" ref-type="bibr">2001</xref>; Nonaka et al., <xref rid="B121" ref-type="bibr">2001</xref>; Durgan et al., <xref rid="B37" ref-type="bibr">2005</xref>, <xref rid="B38" ref-type="bibr">2007</xref>; Takeda et al., <xref rid="B159" ref-type="bibr">2007</xref>). Peripheral clocks have their own regulatory mechanisms, which are specific to each peripheral organ by regulating the expression of clock-controlled genes (<italic>Ccg</italic>). CRs have been demonstrated in approximately 8–10% of total genes expressed in mouse heart and liver, more than 90% of them depending on self-autonomous local diurnal oscillators (Storch et al., <xref rid="B153" ref-type="bibr">2002</xref>).</p></sec><sec><title>Genes and proteins</title><p>Important genes are involved in CRs including <italic>Clock</italic> (<italic>Circadian locomotor output cycles kaput</italic>), <italic>Bmal1</italic> (<italic>brain and muscle aryl-hydrocarbon receptor nuclear translocator-like 1</italic>), <italic>Cry1</italic> (<italic>cryptochrome 1</italic>), <italic>Cry2</italic> (<italic>cryptochrome 2</italic>), <italic>Per1</italic> (<italic>Period 1</italic>), <italic>Per2</italic> (<italic>Period 2</italic>), <italic>Per3</italic> (<italic>Period 3</italic>), and <italic>Ccg</italic>. They organize transcription/translation autoregulatory feedback loops comprising both activating and inhibiting pathways (Reppert and Weaver, <xref rid="B136" ref-type="bibr">2002</xref>; Schibler and Sassone-Corsi, <xref rid="B145" ref-type="bibr">2002</xref>). A complex network is formed by all these genes which interlock feedback and forward subtle loops whose complete time course is approximately 24 h. Clock genes Per1, Per2, Bmal1, and Cry1 display rhythmic expression in human hearts (Leibetseder et al., <xref rid="B93" ref-type="bibr">2009</xref>). At the start of the day, transcription of Clock and Bmal1 begins. The proteins CLOCK and BMAL1 are synthesized and then associate as dimers which bind to regulatory DNA sequences (E-box elements) of the promoters of target genes. CLOCK: BMAL1 dimer activates circadian gene transcription of Period genes (Per1, 2, and 3), Chryptochrome genes (Cry 1 and 2), Rev-erb, Ror (related orphan receptor), and Ccg, and drives their rhythmic expression (Reppert and Weaver, <xref rid="B135" ref-type="bibr">2001</xref>, <xref rid="B136" ref-type="bibr">2002</xref>; Young and Kay, <xref rid="B185" ref-type="bibr">2001</xref>; Canaple et al., <xref rid="B19" ref-type="bibr">2006</xref>; Chen and Yang, <xref rid="B23" ref-type="bibr">2014</xref>). Into the cytoplasm, the PER and CRY proteins dimerize and, after translocation to the nucleus, modulate the transcriptional activity of CLOCK: BMAL1 (Kume et al., <xref rid="B89" ref-type="bibr">1999</xref>). Concentrations of BMAL1 and PER proteins cycle in counterpoint. PER2 is a positive regulator of the Bmal1 loop. Protein CRY is a negative regulator of both Per and Cry loops. ROR alpha enhances Bmal1 transcription (Akashi and Takumi, <xref rid="B1" ref-type="bibr">2005</xref>), while the nuclear receptor Rev-erb inhibits it (Ueda et al., <xref rid="B161" ref-type="bibr">2002</xref>). Rev-erb alpha binds to ROR-responsive element (RORE) in the Bmal1 promoter and represses its transcriptional activity (Preitner et al., <xref rid="B131" ref-type="bibr">2002</xref>). Rev-erb alpha protein is a member of the nuclear receptor family of intracellular transcription factors. The gene Rev-erb alpha is a major regulatory component of the circadian clock (Yin et al., <xref rid="B179" ref-type="bibr">2006</xref>) and among various properties, is involved in the circadian expression of plasminogen activator inhibitor type 1 (Wang et al., <xref rid="B168" ref-type="bibr">2006</xref>).</p><sec><title>Circadian rhythms and mutations of genes</title><p>Mutations or deletions of clock genes in mice have shown the key role of circadian clocks to ensure the proper timing of metabolic and cardiovascular processes. There is an increased pathological remodeling and vascular injury together with an aberrant CR in <italic>Bmal1</italic>-knockout and <italic>Clock</italic> mutant mice (Anea et al., <xref rid="B5" ref-type="bibr">2009</xref>). Aortas from <italic>Bmal1</italic>-knockout and <italic>Clock</italic> mutant mice exhibit endothelial dysfunction. Akt (protein kinase B) and subsequent nitric oxide signaling is significantly attenuated in arteries from <italic>Bmal1</italic>-knockout mice. <italic>Bmal1</italic> is a key regulator of myogenesis which may represent a temporal regulatory mechanism to fine-tune myocyte differentiation (Chatterjee et al., <xref rid="B22" ref-type="bibr">2013</xref>). <italic>Bmal1</italic> regulates adipogenesis <italic>via the</italic> Wnt signaling pathway (Guo et al., <xref rid="B60" ref-type="bibr">2012</xref>). Disruption of <italic>Bmal1</italic> in mice led to increased adipogenesis, adipocyte hypertrophy, and obesity. Attenuation of <italic>Bmal1</italic> function resulted in down-regulation of genes in the canonical Wnt pathway known to suppress adipogenesis. Promoters of these genes, i.e., <italic>beta-catenin</italic>, Disheveled <italic>(Dsh)</italic>, T cell-enhancing binding <italic>(Tcf)</italic> display <italic>Bmal1</italic> occupancy, indicating direct circadian regulation by Bmal1. Among several abnormalities, deletion of the clock gene <italic>Bmal1</italic> in mice adipose tissue induces obesity (Paschos et al., <xref rid="B126" ref-type="bibr">2012</xref>). The cardiomyocyte-specific clock mutant <italic>(Ccm)</italic> is a mouse model wherein the cardiomyocyte circadian clock is selectively suppressed (Young et al., <xref rid="B182" ref-type="bibr">2001b</xref>,<xref rid="B183" ref-type="bibr">c</xref>; Durgan et al., <xref rid="B39" ref-type="bibr">2006</xref>). <italic>Ccm</italic> presents a temporal suspension of the cardiomyocyte circadian clock at the wake-to-sleep transition (Young, <xref rid="B180" ref-type="bibr">2009</xref>). Numerous mutations of genes will be discussed in the following paragraphs of this review.</p></sec><sec><title>Circadian rhythms and heart performance</title><p>Loss of synchronization between the internal clock and external stimuli can induce cardiovascular organ damage. Discrepancy in the phases between the central and peripheral clocks also seems to contribute to progression of cardiovascular disorders (Takeda and Maemura, <xref rid="B158" ref-type="bibr">2011</xref>). Peripheral clocks have their own roles specific to each peripheral organ by regulating the expression of <italic>Ccg</italic>, although the oscillation mechanisms of the peripheral clock are similar to that of the SCN (Takeda et al., <xref rid="B159" ref-type="bibr">2007</xref>). Both the physiological and pathological functions of cardiovascular organs are closely related to CRs. Heart rate, blood pressure and endothelial function show diurnal variations within a day. A profound pattern exists in the time of day at which the death may occur (Takeda and Maemura, <xref rid="B158" ref-type="bibr">2011</xref>). The onset of cardiovascular disorders such as acute coronary syndrome, atrial arrhythmias, and subarachnoid hemorrhage exhibits impairment of diurnal oscillations. Stroke and heart attacks most frequently happen in the morning when blood pressure surges.</p><p>Over the course of the day, the normal heart anticipates, responds and adapts to physiological alterations within its environment. Contractile performance, carbohydrate oxidation, fatty acid oxidation (FAO), mitochondrial function, oxygen consumption, and expression of all metabolic genes show diurnal variations. The circadian clock plays an important role in cardiac homeostasis through the anticipation of daily workload. In wild-type mice, the ejection fraction (EF) and the shortening fraction (FS) show circadian variation (Wu et al., <xref rid="B173" ref-type="bibr">2011</xref>). The diurnal variations in EF and FS are altered in mice with disruptions of circadian clock genes and are significantly diminished under an imposed light regimen. The circadian variation in blood pressure and heart rate is disrupted in <italic>Bmal1</italic>(-/-) and <italic>Clock</italic> (mut) mice in which core clock genes are deleted or mutated (Curtis et al., <xref rid="B29" ref-type="bibr">2007</xref>). <italic>Bmal1</italic> deletion abolishes the 24-h frequency in cardiovascular rhythms. However, a shorter ultradian rhythm remains. Sympathetic adrenal function is disrupted in these mice.</p></sec><sec><title>Peroxisome proliferator-activated receptors (PPARs)</title><p>PPARs (alpha, beta/delta, and gamma) are nuclear receptors belonging to the nuclear receptor superfamily. They function as transcription factors within the cell nuclei and regulate the expression of several target genes. PPARs play a pivotal role in various physiological and pathological processes, especially in energy metabolism, development, carcinogenesis, extracellular matrix remodeling, and CRs (Lockyer et al., <xref rid="B101" ref-type="bibr">2009</xref>). PPARs heterodimerize with the retinoid X receptor (RXR). PPARs are activated by their respective ligands, either endogenous fatty acids or pharmaceutical drugs which are potential therapeutic agents. Numerous natural and synthetic compounds, i.e., fatty acids, eicosanoids, arachidonic acid, hypolipidemic fibrates activating PPAR alpha, and anti diabetic thiazolidinediones (TZD) activating PPAR gamma, serve as activators of PPARs. PPARs are involved in numerous pathologies such as obesity, dyslipidemia, insulin resistance, type 2 diabetes, hypertension, cardiac hypertrophy (Berger and Moller, <xref rid="B12" ref-type="bibr">2002</xref>; Kelly, <xref rid="B81" ref-type="bibr">2003</xref>). PPAR beta/delta was not studied in this review.</p></sec><sec><title>PPARs and circadian rhythms</title><p>PPARs integrate the mammalian clock and energy metabolism (Chen and Yang, <xref rid="B23" ref-type="bibr">2014</xref>). PPARs have been shown to be rhythmically expressed in mammalian tissues (Yang et al., <xref rid="B177" ref-type="bibr">2006</xref>) and to directly interact with the core clock genes (Inoue et al., <xref rid="B74" ref-type="bibr">2005</xref>). PPAR beta/delta has not been studied in this review.</p><sec><title>PPAR alpha</title><p>PPAR alpha presents CRs in several organs, i.e. heart, muscles, liver, and kidney (Lemberger et al., <xref rid="B94" ref-type="bibr">1996</xref>; Yang et al., <xref rid="B177" ref-type="bibr">2006</xref>). PPAR alpha expression is stimulated by stress, glucocorticoid hormones, and insulin whose secretion follows CRs (Lemberger et al., <xref rid="B95" ref-type="bibr">1994</xref>). Importantly, PPAR alpha is a direct target of genes (<italic>Bmal1</italic> and <italic>Clock</italic>) through an E-box process (Oishi et al., <xref rid="B122" ref-type="bibr">2005</xref>). The circadian expression of PPAR alpha mRNA is abolished in the liver of homozygous <italic>Clock</italic> mutant mice and is regulated by the peripheral oscillators in a CLOCK-dependent mechanism. In rodent liver, there is a regulatory feedback loop involving BMAL1 and PPAR alpha in peripheral clocks. This regulation occurs via a direct binding of PPAR alpha on a PPAR alpha response element located in the <italic>Bmal1</italic> gene promoter. Moreover, BMAL1 is an upstream regulator of <italic>PPAR alpha</italic> gene expression (Gervois et al., <xref rid="B52" ref-type="bibr">1999</xref>; Canaple et al., <xref rid="B19" ref-type="bibr">2006</xref>). Several genes such as those encoding for sterol regulatory element binding protein, HMG-CoA reductase, fatty acid synthase, are involved in the lipid metabolism. They display circadian fluctuations, and their activities are diminished or suppressed in <italic>PPAR alpha</italic> knockout mice (Patel et al., <xref rid="B128" ref-type="bibr">2001</xref>; Gibbons et al., <xref rid="B53" ref-type="bibr">2002</xref>). PPAR alpha directly regulates the transcriptional activity of <italic>Bmal1</italic> and <italic>Rev-erb alpha</italic> through the PPRE located in the promoter site of their respective genes. <italic>Per2</italic> interacts with nuclear receptors including PPAR alpha and Rev-Erb alpha and serves as a co-regulator of nuclear receptor-mediated transcription. The PPAR alpha agonist fenofibrate increases transcription and resets circadian expression of <italic>Bmal1, Per2, and Rev-erb alpha</italic> in mouse liver (Canaple et al., <xref rid="B19" ref-type="bibr">2006</xref>) and cultured hepatocytes (Gervois et al., <xref rid="B52" ref-type="bibr">1999</xref>). Moreover, bezafibrate can phase advance the rhythmic expression of <italic>Bmal1, Per2, and Rev-erb alpha</italic> in several mouse peripheral tissues (Shirai et al., <xref rid="B149" ref-type="bibr">2007</xref>; Oishi et al., <xref rid="B123" ref-type="bibr">2008</xref>).</p></sec><sec><title>PPAR gamma</title><p>PPAR gamma exhibits variations in diurnal expression in mouse fat, liver, and blood vessels (Yang et al., <xref rid="B177" ref-type="bibr">2006</xref>; Wang et al., <xref rid="B169" ref-type="bibr">2008</xref>). Deletion of <italic>PPAR gamma</italic> in mouse suppresses or diminishes diurnal rhythms (Yang et al., <xref rid="B175" ref-type="bibr">2012</xref>). CRs have been analyzed in two strains of whole-body <italic>PPAR gamma null</italic> mouse models, i.e., <italic>Mox2-Cre</italic> mice (<italic>MoxCre/flox</italic>) or induced by tamoxifen (<italic>EsrCre/flox/TM</italic>). Diurnal variations in blood pressure and heart rate are blunted <italic>in MoxCre/flox</italic> mice. Impaired rhythmicity of the canonical clock genes is observed in adipose tissue and liver. This shows the important role of PPAR gamma in the coordinated control of circadian clocks, metabolism, and cardiac performance (Yang et al., <xref rid="B175" ref-type="bibr">2012</xref>). Moreover, insulin resistance is correlated with a non-dipper type—i.e., with no blood pressure decrease during the circadian cycle- in essential hypertension. TZD are oral hypoglycemic agents act as insulin sensitizers and possess antihypertensive properties. TZD therapy with pioglitazone transforms the CR of blood pressure from a non-dipper to a dipper type (Anan et al., <xref rid="B2" ref-type="bibr">2007</xref>). PPAR gamma contributes to maintain the diurnal variations of both blood pressure and heart rate.</p><p>Rev-Erb alpha, an orphan nuclear receptor and a core clock component, is expressed after PPAR gamma activation with rosiglitazone in rat. Activated PPAR gamma induces <italic>Rev-Erb alpha</italic> promoter activity by binding to the response element <italic>Rev-DR2</italic>. Mutations of the 5′ or 3′ half-sites of the response element suppress PPAR gamma binding and transcriptional activation (Fontaine et al., <xref rid="B45" ref-type="bibr">2003</xref>). PGC-1 alpha, a transcriptional co-activator that regulates energy metabolism, is rhythmically expressed in the liver and skeletal muscle of mice. PGC-1 alpha stimulates the expression of clock genes, notably <italic>Bmal1</italic> and <italic>Rev-erb alpha</italic>, through co-activation of the ROR family of orphan nuclear receptors. Mice lacking PGC-1 alpha show abnormal CRs of activity, body temperature, and metabolic rate (Liu et al., <xref rid="B99" ref-type="bibr">2007a</xref>). <italic>Nocturnin</italic>, a circadian-regulated gene, promotes adipogenesis by stimulating PPAR gamma nuclear translocation (Kawai et al., <xref rid="B80" ref-type="bibr">2010</xref>). Nocturnin binds to PPAR gamma and stimulates its transcriptional activity whereas its deletion suppresses PPAR gamma oscillations (Green et al., <xref rid="B59" ref-type="bibr">2007</xref>). The hormone-dependent interaction of the nuclear receptor RXR alpha with CLOCK negatively regulates CLOCK: BMAL1-mediated transcriptional activation of clock gene expression in vascular cells. RXR alpha can phase shift Per2 mRNA rhythmicity, providing a molecular mechanism for hormonal control of clock gene expression (McNamara et al., <xref rid="B110" ref-type="bibr">2001</xref>).</p></sec></sec><sec><title>Canonical Wnt/beta-catenin pathway</title><p>Beta-catenin plays a key role during epithelial-mesenchymal transition (EMT), that characterizes normal embryonic development, tissue regeneration and cancer proliferation (Heuberger and Birchmeier, <xref rid="B68" ref-type="bibr">2010</xref>). Beta-catenin is a normal constituent of the zonula adherens, a major cell-to-cell adhesion complex in pavement-like tissues. During EMT, the loss of cadherins disrupts the zonula adherens, thus liberating beta-catenin into the cytoplasm. This molecule then migrates to the cell nucleus where it activates the Wnt/beta-catenin target genes. A hallmark of the canonical Wnt pathway activation is the elevation of cytoplasmic beta-catenin protein levels, the subsequent nuclear translocation and further activation of beta-catenin specific gene transcription (Ben-Ze'ev and Geiger, <xref rid="B11" ref-type="bibr">1998</xref>; Klymkowsky et al., <xref rid="B84" ref-type="bibr">1999</xref>; Zhurinsky et al., <xref rid="B190" ref-type="bibr">2000</xref>; Moon et al., <xref rid="B114" ref-type="bibr">2002</xref>; Maeda et al., <xref rid="B105" ref-type="bibr">2004</xref>; Sen-Chowdhry et al., <xref rid="B148" ref-type="bibr">2005</xref>; Garcia-Gras et al., <xref rid="B49" ref-type="bibr">2006</xref>), (Figure <xref ref-type="fig" rid="F1">1</xref>). In the absence of Wnt ligands, beta-catenin is recruited into a destruction complex that contains adenomatous polyposis coli (APC) and Axin, which facilitate the phosphorylation of beta-catenin by glycogen synthase kinase 3- beta (GSK3-beta). GSK3-beta phosphorylates the N-terminal domain of beta-catenin, thereby targeting it for ubiquitination and proteasomal degradation. In the presence of a Wnt ligand, the binding of Wnt to Frizzled (Fzd) leads to activation of the phosphoprotein Disheveled (Dsh). Dsh recruits Axin and the destruction complex to the plasma membrane, where Axin directly binds to the cytoplasmic tail of LRP5/6. Axin is degraded, which decreases beta-catenin degradation. The activation of Dsh also leads to the inhibition of GSK3-beta by phosphorylation, which further reduces the phosphorylation and degradation of beta-catenin. The beta-catenin degradation complex is inactivated with recruitment of axin to the plasma membrane, thus stabilizing the non-phosphorylated beta-catenin which translocates to the nucleus. Beta-catenin binds to T cell/lymphoid-enhancing binding (Tcf/Lef) transcription factors. The resulting complex becomes active by displacing Grouchos, leading to activation of numerous target genes.</p><fig id="F1" position="float"><label>Figure 1</label><caption><p><bold>The Wnt/beta-catenin pathway. (A)</bold> In the absence of Wnt, cytosolic beta-catenin is phosphorylated by GSK3 beta. APS and AXIN complex with GSK3 beta and beta-catenin to enhance the destruction process into the proteasome. Phosphorylated beta-catenin is recognized by the ubiquitin ligase beta -TrCP, ubiquinated and degraded. The Wnt pathway is in an “off state.” <bold>(B)</bold> In the presence of Wnt, Wnt binds both Frizzled and LRP5/6 receptors to initiate GRK5/6-mediated LRP phosphorylation and disheveled-mediated Frizzled internalization. Disheveled membrane translocation leads to dissociation of the AXIN/APC/GSK3 beta complex. Beta-catenin phosphorylation is inhibited and accumulates into the cytosol. Beta-catenin then translocates to the nucleus to bind Lef-Tcf co-transcription factors, which induces the Wnt-response gene transcription. Abbreviations: APC, adenomatous polyposis coli; Dsh, Disheveled; GSK3 beta, glycogen synthase kinase 3 beta; LRP5/6, low density lipoprotein receptor-related protein 5/6; Fzd, Frizzled.</p></caption><graphic xlink:href="fphys-05-00429-g0001"></graphic></fig></sec><sec><title>Canonical Wnt/beta-catenin pathway and PPAR gamma</title><p>Numerous studies have shown the direct interaction between beta-catenin and PPAR gamma (Moldes et al., <xref rid="B113" ref-type="bibr">2003</xref>; Jansson et al., <xref rid="B78" ref-type="bibr">2005</xref>; Garcia-Gras et al., <xref rid="B49" ref-type="bibr">2006</xref>). PPAR gamma activation inhibits the beta-catenin activation of Tcf/Lef transcription factors (Lu and Carson, <xref rid="B103" ref-type="bibr">2010</xref>). The TZD PPAR gamma agonists troglitazone, rosiglitazone, and pioglitazone, and the non-TZD PPAR gamma activator GW1929 inhibit the beta-catenin-induced transcription in a PPAR gamma dependent manner. Activation of the Wnt-beta catenin pathway leads to osteogenesis, not adipogenesis and its inhibition leads to an increase in transcription of PPAR gamma. Osteogenic pathway is linked to the stimulation of Wnt signal leading to the final transcriptional activation of early osteogenic markers such as RUNX-2 and ALP, mediated by beta-catenin. Conversely, the adipogenic pathway involves inhibition of Wnt pathway leading to ubiquitination/degradation of beta-catenin which results in the transcription of PPAR gamma, a pivotal initiator of adipogenesis. The canonical Wnt/beta-catenin-PPAR gamma system determines the molecular switching of osteablastogenesis vs. adipogenesis (Takada et al., <xref rid="B157" ref-type="bibr">2009</xref>). PPAR gamma is a prime inducer of adipogenesis that inhibits osteoblastogenesis. Two different pathways switch the cell fate decision from adipocytes to osteoblasts by suppressing the transactivation function of PPAR gamma. TNF-alpha- and IL-1-induced TAK1/TAB1/NIK signaling cascade attenuate PPAR gamma-mediated adipogenesis by inhibiting the binding of PPAR gamma to the DNA response element. PPAR gamma suppresses Wnt/beta-catenin signaling during adipogenesis (Moldes et al., <xref rid="B113" ref-type="bibr">2003</xref>). Wnt/beta-catenin pathway operates to maintain the undifferentiated state of preadipocytes by inhibiting adipogenic gene expression. Importantly, there is a reciprocal relationship between beta-catenin expression and PPAR gamma activity.</p></sec><sec><title>Diseases associated with deactivation of the Wnt/beta-catenin pathway and increased expression of PPAR gamma</title><p>Numerous diseases present a common denominator: activation of the Wnt/beta-catenin pathway decreased and the expression of PPAR gamma increased. In most cases, expression of PPAR alpha decreases.</p><sec><title>Arrhythmogenic right ventricular cardiomyopathy (ARVC)</title><p>ARVC is a rare human disease characterized by the development of a fibro-fatty tissue in both ventricles, prominently involving the right ventricular (RV) myocardium (Marcus et al., <xref rid="B107" ref-type="bibr">1982</xref>; Fontaine et al., <xref rid="B46" ref-type="bibr">1999</xref>) (Figure <xref ref-type="fig" rid="F2">2</xref>). Cardiac dysfunction progressively develops, initially located at the RV and becoming biventricular in about 20% of cases (Richardson et al., <xref rid="B137" ref-type="bibr">1996</xref>; Hebert et al., <xref rid="B65" ref-type="bibr">2004</xref>). ARVC is most often an autosomic family-related disease. Genetic mutations have been identified in about 50% of cases, occurring among the five desmosomal proteins so far identified in the ventricular cardiomyocyte, i.e., desmoglein 2 (DSG2), desmocollin 2 (DSC2), plakophilin 2 (PKP2), plakoglobin (PG), and desmoplakin (DSP) (Basso et al., <xref rid="B8" ref-type="bibr">2009</xref>; Fressard et al., <xref rid="B47" ref-type="bibr">2010</xref>). PPAR abnormalities have been reported in ARVC with an increase in PPAR gamma and a decrease in PPAR alpha in RV (Djouadi et al., <xref rid="B32" ref-type="bibr">2009</xref>).</p><fig id="F2" position="float"><label>Figure 2</label><caption><p><bold>Arrhythmogenic right ventricular cardiomyopathy (ARVC) histology. (A)</bold> Typical morphology of right ventricular transmural free wall section in a terminal ARVC heart transplant specimen, showing extensive fibro-fatty replacement. A mid-mural residual muscular core (black asterisk) is well-identified. Fibrosis is prominently located at the subendocardium. Note the layer of normal subepicardial fat (Hematoxylin Eosin Saffron staining, original magnification × 10). <bold>(B–D)</bold> are fresh tissue snap frozen fragments representative of regions referred to as muscular <bold>(B,C)</bold> and fatty myocardium, <bold>(D)</bold> respectively, stained with oil red O (original magnification × 50). The red staining indicates neutral lipid accumulation. <bold>(B)</bold> Note the normal discrete perinuclear staining of the cardiomyocytes (white arrow) within the well-preserved myocardial core. <bold>(C)</bold> In contrast, there is an abnormal major accumulation of fatty droplets (not visible under standard staining) dispersed within the cells of the mid mural muscular zone located above the residual muscular core and surrounded by fatty tissue. Note the remaining normal central position of the nucleus within the myocardial cells (red arrow). <bold>(D)</bold> Finally, there is a direct transdifferentiation of myocardial cells into adipocytes within the upper muscular zone bordering the normal subepicardial fat. Take notice of the major confluence of the fatty droplets as well as of the final aspect of total fatty transformation with migration of the nucleus beneath the cell membrane (black arrows).</p></caption><graphic xlink:href="fphys-05-00429-g0002"></graphic></fig><p>Molecular mechanisms underlying ARVC are now better understood. The link between PPAR gamma dysfunction and desmosomal genetic mutations implicates the Wnt/beta-catenin pathway. Thus, the suppression of canonical Wnt/beta-catenin signaling by nuclear PG recapitulates the phenotype of ARVD by exhibiting fat accumulation in cardiomyocytes, enhanced myocyte apoptosis, ventricular dysfunction, and ventricular arrhythmias in transgenic mice (Garcia-Gras et al., <xref rid="B49" ref-type="bibr">2006</xref>). The desmosomal PG also known as gamma-catenin, has structural and functional similarities to beta-catenin, which is the effector for canonical Wnt signaling (Moon et al., <xref rid="B114" ref-type="bibr">2002</xref>). PG interacts and competes with beta-catenin at multiple cellular levels with a net negative effect on the canonical Wnt/beta-catenin signaling pathway through Tcf/Lef transcription factors (Ben-Ze'ev and Geiger, <xref rid="B11" ref-type="bibr">1998</xref>; Klymkowsky et al., <xref rid="B84" ref-type="bibr">1999</xref>; Zhurinsky et al., <xref rid="B190" ref-type="bibr">2000</xref>; Maeda et al., <xref rid="B105" ref-type="bibr">2004</xref>). Mutating the desmosomal protein DSP by impairing desmosome assembly set free gamma-catenin from the desmosomes. As a consequence, gamma catenin translocates to the nucleus and after competition with beta-catenin suppresses signaling through the canonical Wnt/beta-catenin-Tcf/Lef pathway. Suppression of DSP expression responsible for human ARVC, leads to nuclear localization of PG and to suppression of canonical Wnt/beta-catenin-Tcf/Lef1 signaling in cultured atrial myocytes and in mouse hearts (Sen-Chowdhry et al., <xref rid="B148" ref-type="bibr">2005</xref>). Tcf/Lef1 suppression induces a transcriptional switch from myogenesis to adipogenesis (Ross et al., <xref rid="B139" ref-type="bibr">2000</xref>). This leads to enhanced adipogenesis, fibrogenesis, and myocyte apoptosis, thus summarizing the phenotype of human ARVC (Corrado et al., <xref rid="B28" ref-type="bibr">1997</xref>).</p></sec><sec><title>Cardiac hypoxia</title><p>Hypoxia up-regulates expression of <italic>PPAR gamma angiopoietin-related</italic> gene in cardiomyocytes (Belanger et al., <xref rid="B9" ref-type="bibr">2002</xref>). Hypoxia-inducible factor 1 alpha (HIF1 alpha) inhibits PPAR alpha expression during hypoxia (Narravula and Colgan, <xref rid="B119" ref-type="bibr">2001</xref>). Hypoxia leads to activation of HIF1 alpha (Krishnan et al., <xref rid="B88" ref-type="bibr">2009</xref>) and several genes involved in the regulation of glucose transporters, glycolytic enzyme, and pyruvate deshydrogenase kinase (PDK1). HIF1 alpha overexpression <italic>in vitro</italic> leads to triacylglycerol accumulation, and reduced FAO due to inhibition of PPAR alpha. Cardiac hypoxia represents a pathological state where expression of PPAR alpha is reduced whereas that of PPAR gamma is increased. Hypoxia triggers a cascade of cellular metabolic responses including a decrease in mitochondrial oxidative flux (Huss et al., <xref rid="B72" ref-type="bibr">2001</xref>). Under hypoxic conditions, myocytes exhibit significant accumulation of intracellular neutral lipid consistent with reduced carnitine palmitoyltransferase-1 (CPT-1) activity and diminished FAO capacity. Hypoxia reduces PPAR alpha/RXR binding activity and had no effect on the nuclear level of PPAR alpha protein. Hypoxia reduced the nuclear and cellular RXR levels and deactivates PPAR alpha by reducing the availability of its obligate partner RXR. In rat models of systemic hypoxia (Razeghi et al., <xref rid="B134" ref-type="bibr">2001</xref>), cardiac hypoxia induces a decrease in heart muscle transcript levels of <italic>PPAR alpha</italic> and <italic>PPAR alpha-regulated</italic> genes (PDK4), muscle CPT-1, and malonyl-CoA decarboxylase. This explains the increased reliance of the heart for glucose during hypoxia.</p><p>PPAR gamma co-activator 1 alpha (PGC-1 alpha) is a major regulator of mitochondrial biogenesis and activity in the cardiac muscle. Hypoxia stimulates the expression of PGC-1 alpha in cardiac myocytes (Zhu et al., <xref rid="B189" ref-type="bibr">2010</xref>). PGC-1 alpha stimulates the expression of clock genes, particularly <italic>Bmal1</italic> and <italic>Rev</italic>-<italic>erb alpha</italic> (Liu et al., <xref rid="B99" ref-type="bibr">2007a</xref>). Mice lacking PGC-1alpha present abnormal diurnal rhythms of activity, body temperature, and metabolic rate. Overexpression of PGC-1 alpha inhibits clock gene expression in both heart and skeletal muscles and decreases the expression of PPAR alpha. PGC-1 alpha overexpression abolishes the diurnal variation of EF (Wu et al., <xref rid="B173" ref-type="bibr">2011</xref>) and plays an important role on cardiac function by regulating CRs of metabolic genes.</p><p>Ephrins belong to the family of receptor tyrosine kinases. Interestingly, Ephrin-Eph cell signaling is linked to the Wnt/beta catenin pathway (Clevers and Batlle, <xref rid="B26" ref-type="bibr">2006</xref>) and favorably influences cardiomyocyte viability which ultimately preserves cardiac function after myocardial infarction. Ephrin-Eph signaling could potentially be a new therapeutic target in the treatment of myocardial infarction (O'Neal et al., <xref rid="B124" ref-type="bibr">2013</xref>). In non re-perfused hearts of mice with a functional deletion of the CR gene <italic>mPer2</italic>, myocardial infarct size is reduced. A decrease in infarct size in <italic>mPer2-M</italic> mouse hearts following ischemia-reperfusion injury and ischemic preconditioning is observed and improves preservation of myocardial viability. In the <italic>mPer2</italic>-mutant mouse myocardium cardio-protection occurs via the mechanisms connecting cardiac events, mitochondrial function, and <italic>mPer2</italic> (Virag et al., <xref rid="B164" ref-type="bibr">2013</xref>).</p></sec><sec><title>Cardiac hypertrophy and cardiac overload</title><p>Development of cardiac hypertrophy and progression to heart failure induce a change in myocardial metabolism, characterized by a switch from fatty acid utilization to glycolysis, and lipid accumulation. PPAR gamma and HIF-1 alpha are key mediators of lipid anabolism and glycolysis, respectively. They are jointly up-regulated in hypertrophic cardiomyopathy and cooperate to mediate key changes in cardiac metabolism (Krishnan et al., <xref rid="B88" ref-type="bibr">2009</xref>). In response to pathological stress, HIF-1 alpha activates glycolytic genes, and PPAR gamma. This results in increased glycolytic flux, glucose-to-lipid conversion via the glycerol-3-phosphate pathway, and contractile dysfunction. Ventricular deletion of HIF1 alpha in mice prevents hypertrophy-induced PPAR gamma activation, the consequent metabolic re-programming, and contractile dysfunction. HIF-1 alpha and PPAR gamma protein expression is up-regulated in human and mouse cardiac hypertrophy. HIF 1 alpha directly activates PPAR gamma transcription. PPAR gamma is a key downstream effector of HIF-1 alpha-driven triacylglycerol accumulation in cardiomyocytes (Krishnan et al., <xref rid="B88" ref-type="bibr">2009</xref>).</p><p>In pathological hypertrophied heart, PPAR alpha expression and activity are diminished, leading to a reduction in the capacity for FAO and increased rate of glucose utilization (Barger et al., <xref rid="B7" ref-type="bibr">2000</xref>). Alpha 1-adrenergic agonist-induced hypertrophy of cardiomyocytes in culture results in a switch in energy substrate preference from fatty acids to glucose and in a significant decrease in palmitate oxidation rates together with a reduction in the expression of the gene encoding muscle carnitine palmitoyltransferase 1 (<italic>M-CPT1</italic>). Cardiac myocyte transfection has shown that <italic>M-CPT1</italic> promoter activity is repressed during cardiomyocyte hypertrophic growth, an effect involving a <italic>PPAR alpha</italic> response element. Hypertrophied myocytes exhibited reduced capacity for cellular lipid homeostasis, as evidenced by intracellular fat accumulation. Thus, during cardiomyocyte hypertrophic growth, PPAR alpha is deactivated at several levels, leading to diminished capacity for myocardial lipid metabolism. The functional consequences of this metabolic switch from lipid to glucose may serve to preserve ventricular function in the context of chronic pressure overload (Young et al., <xref rid="B181" ref-type="bibr">2001a</xref>). During cardiac pressure overload-induced cardiac hypertrophy, the diurnal variation of metabolic gene expression is completely suppressed and the cardiac performance is impaired (Young et al., <xref rid="B182" ref-type="bibr">2001b</xref>). The induction of clock output genes is attenuated in the pressure-overloaded hypertrophied heart, providing evidence for a diminished ability of the hypertrophied heart to anticipate and subsequently to adapt to physiological alterations during the day (Young et al., <xref rid="B183" ref-type="bibr">2001c</xref>).</p></sec><sec><title>Osteoporosis</title><p>The Wnt pathway induces differentiation of bone-forming cells (osteoblasts) and suppresses the development of bone-resorbing cells (osteoclasts). It is controlled by antagonists that interact either with Wnt proteins (Wnts) or with Wnt co-receptors. Wnts function as key regulators in osteogenic differentiation of mesenchymal stem cells and bone formation. Aberrant Wnt pathways are associated with many osteogenic diseases (Rawadi and Roman-Roman, <xref rid="B133" ref-type="bibr">2005</xref>; Canalis, <xref rid="B18" ref-type="bibr">2013</xref>). Both human genetics and animal studies have pointed out the role of the Wnt/LRP5 pathway as a major regulator of bone mass. In mice, down-regulation or neutralization of Wnt antagonists enhances bone formation. Mutations in <italic>LRP5</italic> cause primary osteoporosis by reducing Wnt signaling activity and result in decreased bone formation (Korvala et al., <xref rid="B86" ref-type="bibr">2012</xref>). Heterozygous PPAR gamma-deficient mice exhibit high bone mass by stimulating osteoblastogenesis from bone marrow progenitors. Inhibition of PPAR gamma increases osteoblastogenesis and bone mass in male C57BL/6 Mice (Duque et al., <xref rid="B36" ref-type="bibr">2013</xref>). PPAR gamma inhibits osteoblast differentiation (Wan et al., <xref rid="B167" ref-type="bibr">2007</xref>).</p><p>Cardiovascular disease and osteoporosis are common age-related conditions associated with significant morbidity and mortality. An increasing body of biological and epidemiological evidences provides support for a link between cardiovascular disease and osteoporosis that cannot be explained by age alone (Farhat and Cauley, <xref rid="B41" ref-type="bibr">2008</xref>). Several hypotheses have been proposed to explain the link between osteoporosis and cardiovascular disease including shared risk factors, common pathophysiological mechanisms and common genetic factors.</p></sec><sec><title>Alzheimer disease (AD)</title><p>AD is a progressive neurodegenerative disorder, neuropathologically characterized by amyloid-beta (Abeta) plaques, and hyperphosphorylated tau accumulation with hereditary missense mutations in the amyloid precursor protein or presenilin-1 and -2 (<italic>PSEN1</italic> and <italic>PSEN2</italic>) genes. Presenilins are involved in modulating beta-catenin stability; therefore familial AD-linked PSEN-mediated effects can reduce the Wnt pathway (Boonen et al., <xref rid="B13" ref-type="bibr">2009</xref>). Tau phosphorylation is mediated by GSK-3 beta, a key antagonist of the Wnt pathway. Sustained loss of function of Wnt/beta-catenin signaling underlies the onset and progression of AD (Inestrosa and Toledo, <xref rid="B73" ref-type="bibr">2008</xref>; De Ferrari et al., <xref rid="B30" ref-type="bibr">2014</xref>). Downregulation of Wnt signaling induced by Abeta is associated with AD progression. Persistent activation of Wnt signaling through Wnt ligands, or inhibition of negative regulators of Wnt signaling, such as Dickkopf-1 and GSK-3 beta are able to protect against Abeta toxicity and ameliorate cognitive performance in AD (Wan et al., <xref rid="B166" ref-type="bibr">2014</xref>). A relationship between amyloid-beta-peptide -induced neurotoxicity and a decrease in the cytoplasmatic levels of beta-catenin has been observed. Although PPAR gamma is elevated in the brain of AD individuals (Jiang et al., <xref rid="B79" ref-type="bibr">2008</xref>), activation of the Wnt signaling pathway may be proposed as a therapeutic target for the treatment of AD.</p><p>In old mice engineered to lack <italic>Bmal1</italic>, there is evidence of brain cell damage that looked similar to that seen in AD. BMAL1 in a complex with CLOCK regulates cerebral redox homeostasis and connects impaired clock gene function to neurodegeneration (Musiek et al., <xref rid="B116" ref-type="bibr">2013</xref>). Altered CR synchronization has been reported in the brain of AD patients (Cermakian et al., <xref rid="B20" ref-type="bibr">2011</xref>). CR disturbances affect as many as a quarter of AD patients. Alterations in the SCN and melatonin secretion are the major factors linked with CR abnormalities. Daytime agitation, night-time insomnia, and restlessness are among the common behavioral alterations observed in AD. Normally, in the interstitial fluid, Abeta has a diurnal fluctuation with low levels during sleep and peak levels during wake. Prolonged wake and/or orexin administration increase levels of the Abeta in the interstitial fluid of the brain in mice. Orexin antagonist reduces amyloid deposits in brain areas. There is a strong causal association between AD and cardiovascular disease. Several cardiovascular risk factors including hypertension and diabetes are also risk factors for dementia (Stampfer, <xref rid="B152" ref-type="bibr">2006</xref>).</p></sec><sec><title>Bipolar disorder and schizophrenia</title><p>The Wnt pathway and its key enzyme, GSK 3 beta, which antagonizes the canonical Wnt pathway, play an important role in regulating synaptic plasticity, cell survival, and CRs in the mature central nervous system. This pathway is implicated in the pathophysiology and treatment of bipolar disorder (Gould and Manji, <xref rid="B58" ref-type="bibr">2002</xref>; Valvezan and Klein, <xref rid="B162" ref-type="bibr">2012</xref>). GSK3- beta-inhibitor lithium chloride enhances activation of Wnt canonical signaling (Hedgepeth et al., <xref rid="B66" ref-type="bibr">1997</xref>; Sinha et al., <xref rid="B151" ref-type="bibr">2005</xref>; Galli et al., <xref rid="B48" ref-type="bibr">2013</xref>). Lithium activates downstream components of the Wnt signaling pathway <italic>in vivo</italic>, leading to an increase of the beta-catenin protein. GSK3-beta phosphorylates and stabilizes the orphan nuclear receptor Rev-erb alpha, a negative component of the circadian clock. Lithium treatment of cells leads to rapid proteasomal degradation of Rev-erb alpha and activation of clock gene <italic>Bmal1</italic> (Yin et al., <xref rid="B179" ref-type="bibr">2006</xref>). The origin of cyclicity in bipolar disorders has been shown by means of a computational approach, and this disease enters the class of dissipative structures (Goldbeter, <xref rid="B56" ref-type="bibr">2013</xref>). Valproate, an effective medication for the prevention and treatment of mood symptoms in bipolar disorder causes a decrease of PPAR gamma signaling (Lan et al., <xref rid="B90" ref-type="bibr">2008</xref>). Many cardiovascular complications are seen in bipolar disorder (Swartz and Fagiolini, <xref rid="B156" ref-type="bibr">2012</xref>).</p><p>An emerging role for Wnt and GSK-3 beta signaling pathways has been found in schizophrenia (Singh, <xref rid="B150" ref-type="bibr">2013</xref>). Sleep and circadian rhythm disruption are seen in schizophrenia (Wulff et al., <xref rid="B174" ref-type="bibr">2012</xref>). Schizophrenia increases risks of cardiovascular disease, particularly coronary heart disease, dyslipidemia, diabetes and hypertension (Hennekens et al., <xref rid="B67" ref-type="bibr">2005</xref>; Andreassen et al., <xref rid="B3" ref-type="bibr">2013</xref>).</p></sec></sec><sec><title>Diseases associated with activation of the Wnt/beta-catenin pathway and decreased expression of PPAR gamma</title><p>Numerous diseases present a common denominator: the Wnt/beta-catenin pathway is overexpressed and the PPAR gamma expression is decreased. This explains why type 2 diabetes is commonly associated with hypertension, sympathetic- parasympathetic abnormalities, and cancers and why CR disruptions are often observed among these pathologies. PPAR alpha expression is often increased in these diseases.</p><sec><title>Impaired sympathetic-parasympathetic system</title><p>PPAR gamma and sympathetic nerve activity (SNA) antagonistically regulate energy metabolism and cardiovascular function with the former promoting anabolism and vasorelaxation and the later favoring catabolism and vasoconstriction (Yang et al., <xref rid="B176" ref-type="bibr">2013</xref>). Systemic inactivation of PPAR gamma can be generated constitutively by using Mox2-Cre mice (<italic>MoxCre/flox</italic>) or inducibly by using the tamoxifen system (<italic>EsrCre/flox/TM</italic>). There is an increase in heart rate in both strains of null mice. PPAR gamma deletion causes the activation of SNA. Rosuvastatin increases vascular endothelial PPAR gamma expression and corrects blood pressure variability in obese dyslipemic mice (Desjardins et al., <xref rid="B31" ref-type="bibr">2008</xref>). Sympathetic adrenal function is disrupted in both <italic>Bmal1(-/-)</italic> and <italic>Clock</italic> (mut) mice (Curtis et al., <xref rid="B29" ref-type="bibr">2007</xref>). Although a shorter ultradian rhythm remains, <italic>Bmal1</italic> deletion abolishes the 24-h frequency in cardiovascular rhythms. In humans, heart rate variability has been shown to be driven by an intrinsic mechanism (Hu et al., <xref rid="B71" ref-type="bibr">2004</xref>; Ivanov et al., <xref rid="B76" ref-type="bibr">2007</xref>). CRs and sleep modulate the sympathetic-parasympathetic balance. Sleep deprivation induces a decrease in the global variability, and an imbalance of the autonomous nervous system (ANS) with an increase in sympathetic activity and a loss of parasympathetic predominance. Human individuals homozygous for the longer allele PER3(5/5) compared with PER3(4/4) subjects present an elevated sympathetic predominance and a reduction of parasympathetic activity (Viola et al., <xref rid="B163" ref-type="bibr">2008</xref>). In mice, selective deletion of the <italic>Bmal1</italic> activator PPAR gamma in the vasculature induces a diminution in heart rate circadian variations (Wang et al., <xref rid="B169" ref-type="bibr">2008</xref>). The CCM mouse model exhibits a decrease in heart rate. Conversely, this model does not present differences in systolic, diastolic, and mean blood pressures as compared with controls (Bray et al., <xref rid="B15" ref-type="bibr">2008</xref>).</p></sec><sec><title>Type 2 diabetes</title><p>PPAR alpha activity and its downstream targets are abnormally activated in the diabetic heart, leading to a marked increase in both fatty acid uptake and oxidation (Finck et al., <xref rid="B42" ref-type="bibr">2005</xref>). Chronic activation of the cardiac PPAR alpha pathway which occurs in the diabetic heart, contributes to myocardial lipid accumulation and diabetic cardiomyopathy (Finck et al., <xref rid="B44" ref-type="bibr">2002</xref>). Diabetes alters the circadian clock in the heart. The clock in the heart loses normal synchronization with its environment during diabetes. Diabetes and fasting activate the expression of cardiac FAO. Excessive fatty acid import and oxidation may be a cause of pathological cardiac remodeling in the diabetic heart (Finck and Kelly, <xref rid="B43" ref-type="bibr">2002</xref>). In type 2 diabetes, PPAR alpha is overexpressed and expression of PPAR gamma is deceased. Some TZD PPAR agonists are used to treat type 2 diabetes. The Wnt/beta-catenin signaling pathway is involved in diabetes mellitus (Ip et al., <xref rid="B75" ref-type="bibr">2012</xref>). Expression of PGC-1 alpha is down-regulated in muscles of type 2 diabetic subjects (Liang and Ward, <xref rid="B98" ref-type="bibr">2006</xref>). PGC-1 alpha activates the expression of insulin-sensitive GLUT4 in skeletal muscle and plays a role in preventing insulin resistance and type 2 diabetes mellitus.</p><p>The mammalian clock (<italic>Bmal1, Clock, Cry1, Cry2, Per1, Per2, and Per3</italic>) expresses CRs and the phases of these CRs are altered in the hearts from streptozotocin-induced diabetic rats (Young et al., <xref rid="B184" ref-type="bibr">2002</xref>). Two BMAL1 haplotypes are associated with type 2 diabetes and hypertension. This provides evidence of a causative role of <italic>Bmal1</italic> variants in pathological components of the metabolic syndrome (Woon et al., <xref rid="B172" ref-type="bibr">2007</xref>). Rhythmic control of insulin release is deregulated in humans with diabetes. Disruption of the clock components <italic>Clock</italic> and <italic>Bmal1</italic> leads to hypoinsulinemia and type 2 diabetes. Pancreatic islets express self-sustained circadian gene and protein oscillations of the transcription factors CLOCK and BMAL1. The phase of oscillation of the islet genes is delayed in circadian mutant mice, and both <italic>Clock</italic> and <italic>Bmal1</italic> mutants show impaired glucose tolerance, reduced insulin secretion and defects in size and proliferation of pancreatic islets (Marcheva et al., <xref rid="B106" ref-type="bibr">2010</xref>). In rodent models of type II diabetes, mean blood pressure is mildly elevated. The elevation in blood pressure is accompanied by changes in the circadian variation of blood pressure as demonstrated in type 2 diabetes (db/db) mice. The daytime fall in blood pressure in mice is significantly blunted in type 2 diabetes db/db mice (Rudic and Fulton, <xref rid="B140" ref-type="bibr">2009</xref>).</p></sec><sec><title>Hypertension</title><p>PPAR gamma in vascular muscle plays a role in the regulation of vascular tone and blood pressure. Thus, mutations in PPAR gamma induce severe hypertension and type 2 diabetes. Transgenic mice with mutations in PPAR gamma in smooth muscle present vascular dysfunction and severe systolic hypertension (Halabi et al., <xref rid="B63" ref-type="bibr">2008</xref>). PPAR gamma ligands lower blood pressure in both animals and humans. PPAR gamma agonist rosiglitazone improves vascular function and lowers blood pressure in hypertensive transgenic mice (Ryan et al., <xref rid="B141" ref-type="bibr">2004</xref>). In mice, after vascular PPAR gamma deletion, circadian variations of blood pressure and heart rate are dampened through a dysregulation of <italic>Bmal1</italic> (Wang et al., <xref rid="B169" ref-type="bibr">2008</xref>). In a null mouse model with specific disruption of PPAR gamma in endothelial cells, PPAR gamma appears to be an important regulator of blood pressure and heart rate mimicking type 2 diabetes, and mediates the antihypertensive effects of rosiglitazone (Nicol et al., <xref rid="B120" ref-type="bibr">2005</xref>). PPAR gamma regulates the renin-angiotensin system activity in the hypothalamic paraventricular nucleus and ameliorates peripheral manifestations of heart failure (Yu et al., <xref rid="B186" ref-type="bibr">2012</xref>). Activation of PPAR gamma down-regulates the renin-angiotensin system. PPAR gamma is expressed in key brain areas involved in cardiovascular and autonomic regulation. Activation of central PPAR gamma reduces sympathetic excitation and improves peripheral manifestations of heart failure by inhibiting brain renin-angiotensin system activity. PPAR gamma ligands lower blood pressure in both animals and humans, possibly via the PPAR gamma-mediated inhibition of the angiotensin II type 1 receptor expression which results in the suppression of the renin-angiotensin system (Sugawara et al., <xref rid="B154" ref-type="bibr">2010</xref>). Genetic variation in BMAL1 is associated with the development of hypertension in man. BMAL1 dysfunction is associated with susceptibility to hypertension and type 2 diabetes. In conditions of constant darkness, <italic>Cry1/Cry2</italic> deficient mice are hypertensive in the daytime (Rudic and Fulton, <xref rid="B140" ref-type="bibr">2009</xref>). Targeted deletion of <italic>Bmal1</italic> in mice <italic>(Bmal1-KO)</italic> abolishes the CR in blood pressure. Mice with targeted deletion of <italic>PPAR gamma</italic> in the endothelium (<italic>EC-PPAR gamma-KO</italic>) exhibit a striking phenotypic resemblance to endothelial cell (EC)-specific deletion of <italic>Bmal1 (EC-Bmal1-KO)</italic>. The loss of PPAR gamma in the aorta of both <italic>EC-PPAR gamma-KO</italic> mice leads to reduced expression of <italic>Bmal1, Cry1, Cry2</italic>, and <italic>Per2</italic>. The ability of PPAR gamma to modulate blood pressure arises in part from its ability to transactivate <italic>Bmal1</italic>.</p></sec><sec><title>Atherosclerosis</title><p>Wnt/beta-catenin signaling plays a key role in atherosclerosis (Wang et al., <xref rid="B170" ref-type="bibr">2002</xref>). Besides Wnt/beta-catenin, GSK3-beta acts as a beta-catenin independent signal, and plays a crucial role in the regulation of cell proliferation and vascular homeostasis. The progression of atherosclerosis is prevented by PPAR gamma ligands in both animals and humans (Sugawara et al., <xref rid="B154" ref-type="bibr">2010</xref>). Monocyte adhesion to vascular endothelium is one of the early processes in the development of atherosclerosis (Lee et al., <xref rid="B92" ref-type="bibr">2006</xref>). Activation of the canonical Wnt/beta-catenin pathway enhances monocyte adhesion to endothelial cells.</p></sec><sec><title>Cardiac-restricted overexpression of PPAR alpha (MHC-PPAR)</title><p>In mice with cardiac-restricted overexpression of PPAR alpha <italic>(MHC-PPAR</italic>), the expression of PPAR alpha target genes is increased whereas that of genes involved in glucose transport and utilization is repressed (Finck et al., <xref rid="B44" ref-type="bibr">2002</xref>). The metabolic phenotype <italic>of MHC-PPAR</italic> mice mimics that of the diabetic heart. <italic>MHC-PPAR</italic> hearts exhibits profiles of diabetic cardiomyopathy including ventricular hypertrophy, activation of gene markers of pathological hypertrophic growth, and systolic ventricular dysfunction. Transgenic mice overexpressing PPAR alpha in muscle (<italic>MCK-PPAR alpha</italic> mice) developed glucose intolerance. Skeletal muscle of <italic>MCK-PPAR alpha</italic> mice exhibits increased FAO rates and reduced insulin-stimulated glucose uptake. The effects on muscle glucose uptake imply transcriptional repression of the <italic>GLUT4</italic> gene.</p></sec><sec><title>Aging</title><p>Aging is associated with various heart diseases, and this may be attributable, in part, to the prolonged exposure of the heart to cardiovascular risk factors. However, aging is also associated with heart disorders such as diastolic dysfunction that are not necessarily linked to the risk factors for cardiovascular diseases. A mechanistic link between Wnt signaling and premature aging or aging-related phenotypes has been demonstrated (Naito et al., <xref rid="B117" ref-type="bibr">2010</xref>). Tissues and organs from klotho-deficient animals showevidence of increased Wnt signaling. Both <italic>in vitro</italic> and <italic>in vivo</italic>, continuous Wnt exposure triggers accelerated cellular senescence. Thus, klotho appears to be a Wnt antagonist (Brack et al., <xref rid="B14" ref-type="bibr">2007</xref>; Liu et al., <xref rid="B100" ref-type="bibr">2007b</xref>). Specific mutations in the human gene encoding lamin A cause premature aging. In mice and humans, these mutations affect adult stem cells by interfering with the Wnt signaling pathway (Meshorer and Gruenbaum, <xref rid="B111" ref-type="bibr">2008</xref>). Overexpression of <italic>Per</italic> in the fruit fly <italic>Drosophila melanogaster</italic> enhances long-term memory, while in <italic>Per</italic> null flies memory is impaired. This supports a link for circadian genes in the processes of learning and memory (Sakai et al., <xref rid="B142" ref-type="bibr">2004</xref>). In aged animals, the normal photonic stimulation of <italic>Per1</italic> expression is reduced. The free-running period of <italic>Per1</italic>–<italic>luc</italic> rhythmicity is shortened in aged animals and the amplitude of <italic>Clock</italic> and <italic>Bmal1</italic> expression is decreased (Kolker et al., <xref rid="B85" ref-type="bibr">2003</xref>).</p></sec><sec><title>Neurodegenerative diseases</title><p>The common denominator overexpression of the Wnt/beta-catenin pathway and the consequent decrease in PPAR gamma expression play a central role in numerous neurodegenerative diseases (Clevers, <xref rid="B24" ref-type="bibr">2006a</xref>; MacDonald et al., <xref rid="B104" ref-type="bibr">2009</xref>; Yang, <xref rid="B178" ref-type="bibr">2012</xref>). PPAR gamma agonists could potentially inhibit neuro-inflammation and subsequently neurodegeneration. This may partially occur through the ability of PPAR: RXR heterodimers to antagonize <italic>NF<sub>κ</sub>B</italic> mediated gene transcription of several inflammatory mediators such as COX-2, iNOS, and various proinflammatory cytokines. It is not surprising that abnormalities of the cardiovascular system and CRs dysfunction are often associated with neurodegenerative pathologies. Sleep disturbances may predict manifestation of neurodegenerative diseases (Postuma and Montplaisir, <xref rid="B130" ref-type="bibr">2009</xref>).</p></sec><sec><title>Huntington disease (HD)</title><p>HD is a dominantly inherited cytosine-adenine-guanine (CAG) repeat disorder with expanded polyglutamine (polyQ) tracts in huntingtin, causing striatal and cortical degeneration (Walker, <xref rid="B165" ref-type="bibr">2007</xref>). Huntingtin interacts with beta-catenin, beta -TrCP, and axin. Normal huntingtin acts as a scaffold protein, promoting the beta-catenin degradation by facilitating the recognition of beta-catenin by beta -TrCP within the destruction complex (Godin et al., <xref rid="B54" ref-type="bibr">2010</xref>). The binding of beta-catenin to the destruction complex is altered in HD. The presence of an abnormal polyQ expansion in mutant huntingtin leads to a decreased binding to beta-catenin therefore impairing the binding of beta-catenin to the destruction complex and subsequently resulting in beta-catenin accumulation into the cytosol. Thus, beta-catenin levels are up-regulated in HD. Mutant huntingtin alters the stability and levels of beta-catenin. Reducing the canonical Wnt signaling pathway confers protection against mutant huntingtin toxicity in Drosophila (Dupont et al., <xref rid="B35" ref-type="bibr">2012</xref>). Knockdown of Wnt ligands improves the survival of HD flies. Overexpression of armadillo/beta-catenin destruction complex component (AXIN, APC2, or GSK3-beta) increases the lifespan of HD flies.</p><p>Early-onset of cardiovascular disease is the second leading cause of death in HD patients. Due to the ubiquitous expression of huntingtin, all cell types with high energetic levels can be impaired. Expression of mutant huntingtin induces cardiac dysfunction in the transgenic model of HD (line R6/2). R6/2 mice develop cardiac dysfunction with cardiac remodeling (e.g. hypertrophy, fibrosis, apoptosis, beta1 adrenergic receptor down-regulation) (Mihm et al., <xref rid="B112" ref-type="bibr">2007</xref>). R6/1 transgenic mice exhibit profound autonomic nervous system-cardiac dysfunction involving both sympathetic and parasympathetic systems, leading to cardiac arrhythmias, and sudden death (Kiriazis et al., <xref rid="B83" ref-type="bibr">2012</xref>). A baroreceptor reflex dysfunction has been described in the BACHD mouse model of HD (Schroeder et al., <xref rid="B147" ref-type="bibr">2011</xref>). Several studies report dysfunction of the autonomic nervous system in HD patients. This may contribute to the increased incidence of cardiovascular events in this patient population that often leads to death. There is a blunted response of the baroreceptor reflex as well as a significantly higher daytime blood pressure in BACHD mice compared to WT controls, which are both indications of autonomic dysfunction. In humans, autonomic dysfunction is present even in the middle stages of HD and affects both the sympathetic and parasympathetic systems (Andrich et al., <xref rid="B4" ref-type="bibr">2002</xref>). Sleep and wake regions of the brain including the brainstem, thalamus, hypothalamus, and cortex are also affected in HD (Kremer et al., <xref rid="B87" ref-type="bibr">1991</xref>). The SCN pacemaker is functional in HD mouse models, so a dysfunction of the circadian circuitry has been proposed to contribute to circadian abnormalities (Pallier and Morton, <xref rid="B125" ref-type="bibr">2009</xref>). Central and peripheral clock gene expression is altered (Maywood et al., <xref rid="B109" ref-type="bibr">2010</xref>). The sleep/wake cycle is disrupted in HD patients characterized by sleep fragmentation at night and delayed sleep phase (Aziz et al., <xref rid="B6" ref-type="bibr">2010</xref>).</p></sec><sec><title>Amyotrophic lateral sclerosis (ALS)</title><p>ALS is a neurodegenerative disease resulting in the progressive loss of upper and lower limb motoneurons and leading to gradual muscle weakening ultimately causing paralysis and death. The Wnt/beta-catenin pathway plays a role in the neurodegeneration of motor neurons in an <italic>in vitro</italic> model of ALS (Pinto et al., <xref rid="B129" ref-type="bibr">2013</xref>). In ALS, a potentially therapeutic pathway may be the activation by PPAR gamma agonists due to their ability to block the neuropathological damage caused by inflammation (Kiaei, <xref rid="B82" ref-type="bibr">2008</xref>). The neuroprotective effect of pioglitazone has been demonstrated in G93A SOD1 transgenic mouse model of ALS and shows a significant increase in their survival. In ALS, PPAR gamma controls natural protective mechanisms against lipid peroxidation (Benedusi et al., <xref rid="B10" ref-type="bibr">2012</xref>).</p><p><italic>Ataxin-2</italic> gene (<italic>ATX2</italic>) is linked to a number of neurodegenerative disorders in humans including ALS and Parkinson disease (PD). ATX2 protein inhibits the production of certain proteins and plays a crucial role in the control of the circadian sleep/wake cycle. <italic>ATX2</italic> regulates the expression of the circadian protein Per in Drosophila. By reducing expression of <italic>ATX2</italic> in Drosophila, the flies are active two and half hours longer. Patients suffering from a form of the neurodegenerative disease spinocerebellar ataxia caused by <italic>ATX2</italic> mutations also experience rapid eye movement sleep disruptions. <italic>ATX2</italic> is necessary for PER accumulation in circadian pacemaker neurons and thus determines period length of circadian behavior. ATX2 is required for the function of TWENTY-FOUR, an activator of PER translation. In humans with ALS, CR of cortisol is impaired (Patacchioli et al., <xref rid="B127" ref-type="bibr">2003</xref>). Both sympathetic and parasympathetic dysfunctions are observed in ALS (Druschky et al., <xref rid="B34" ref-type="bibr">1999</xref>). There are sleep-wake disturbances in patients with ALS (Lo Coco et al., <xref rid="B102" ref-type="bibr">2011</xref>). In human ALS, heart failure is a frequent common cause of death (Gdynia et al., <xref rid="B50" ref-type="bibr">2006</xref>).</p></sec><sec><title>Parkinson disease (PD)</title><p>In a mouse model of PD, a cross talk between inflammatory and Wnt/beta-catenin signaling pathways is involved (L'Episcopo et al., <xref rid="B97" ref-type="bibr">2012</xref>). The Wnt1 regulated Frizzled-1/beta-catenin signaling pathway controls the mesencephalic dopaminergic neuron-astrocyte crosstalk (L'Episcopo et al., <xref rid="B96" ref-type="bibr">2011</xref>). The PPAR gamma agonist pioglitazone modulates inflammation and induces neuroprotection in PD monkeys (Swanson et al., <xref rid="B155" ref-type="bibr">2011</xref>) and mice (Schintu et al., <xref rid="B146" ref-type="bibr">2009</xref>). Expanded glutamine repeats of the ATX2 protein have been identified in fronto-temporal lobar degeneration in PD (Ross et al., <xref rid="B138" ref-type="bibr">2011</xref>). Moreover, a peripheral molecular clock, as reflected in the dampened expression of the clock gene <italic>Bmal1</italic> in leukocytes is altered in PD patients (Cai et al., <xref rid="B17" ref-type="bibr">2010</xref>). There is a disappearance of CRs in a PD dog model (Hineno et al., <xref rid="B69" ref-type="bibr">1992</xref>). Sleep disturbances in PD may be related to CR dysfunction (Hack et al., <xref rid="B62" ref-type="bibr">2014</xref>). Sleep complaints are present in almost half of PD patients. PD patients exhibit increased sleep latency and reduced sleep efficiency. In PD, there is a sustained elevation of serum cortisol levels, reduced circulating melatonin levels, and altered <italic>Bmal1</italic> expression (Breen et al., <xref rid="B16" ref-type="bibr">2014</xref>). PD causes dysfunction of the diurnal autonomic cardiovascular regulation. This dysfunction is profound in patients with severe PD (Haapaniemi et al., <xref rid="B61" ref-type="bibr">2001</xref>).</p></sec><sec><title>Multiple sclerosis (MS)</title><p>Wnt signaling is involved in the MS pathogenesis (Yuan et al., <xref rid="B187" ref-type="bibr">2012</xref>). Mice with experimental autoimmune encephalomyelitis (EAE) have been widely used as a MS model with central nervous system demyelination, neuro-inflammation, and motor impairments. Wnt3a, a Wnt ligand for the canonical pathway, is significantly increased in the spinal cord dorsal horn (SCDH) of the EAE mice. Beta-catenin is also significantly up-regulated. Wnt signaling pathways are up-regulated in the SCDH of the EAE mice and aberrant activation of Wnt signaling contributes to the development of EAE-related chronic pain. PPAR gamma agonists modulate the development of experimental EAE (Drew et al., <xref rid="B33" ref-type="bibr">2008</xref>). Moreover, the risk of myocardial infarction, stroke, heart failure, and atrial fibrillation or flutter is increased in MS patients (Jadidi et al., <xref rid="B77" ref-type="bibr">2013</xref>).</p></sec><sec><title>Friedreich ataxia (FRDA)</title><p>FRDA is a debilitating, life-shortening, degenerative neuromuscular disorder, due to frataxin (FXN) deficiency. FRDA is characterized by neuronal degeneration and heart failure, which are due to loss of transcription of the <italic>FXN</italic> gene caused by a trinucleotide repeat expansion. FXN is a mitochondrial protein involved in iron–sulfur-cluster biogenesis, serving to bind and transfer iron to key electron transport complexes and cytochrome C. Diabetes mellitus and serious heart dysfunction (hypertrophic cardiomyopathy) are associated in most cases. The PPAR gamma agonist Azelaoyl PAF increases FXN protein and mRNA expression in human neuroblastoma cells SKNBE and in primary fibroblasts from skin biopsies from FRDA patients. This offers new implications for the FRDA therapy (Marmolino et al., <xref rid="B108" ref-type="bibr">2009</xref>). It has been shown a coordinate dysregulation of the PPAR gamma co-activator PGC-1 alpha and transcription factor Srebp1 in cellular and animal models of FXN deficiency, and in cells from FRDA patients. A genetic modulation of the PPAR gamma pathway affects FXN levels <italic>in vitro</italic>, supporting PPAR gamma as a new therapeutic target in FRDA (Coppola et al., <xref rid="B27" ref-type="bibr">2009</xref>).</p></sec><sec><title>Colon cancer</title><p>Activation of beta-catenin-Tcf signaling has been observed in colon cancer (Morin et al., <xref rid="B115" ref-type="bibr">1997</xref>). Activation of the Wnt signaling pathway via mutation of the <italic>APC</italic> gene is a critical event in the development of colon cancer (Najdi et al., <xref rid="B118" ref-type="bibr">2011</xref>). Inherited mutations in <italic>APC</italic> lead to the development of non-invasive colonic adenomas (polyps). Wnt pathway activation is a driving force in the development of adenomas. Activation of the Wnt/beta-catenin signaling pathway decreases PPAR gamma activity in colon cancer cells (Jansson et al., <xref rid="B78" ref-type="bibr">2005</xref>) and a loss-of-function mutations in PPAR gamma is associated with human colon cancer (Sarraf et al., <xref rid="B143" ref-type="bibr">1999</xref>).</p><p>Colorectal cancer is linked to CR dysregulation (Savvidis and Koutsilieris, <xref rid="B144" ref-type="bibr">2012</xref>). Down-regulation of <italic>Per2</italic> increases beta-catenin protein levels and its target cyclin D, leading to cell proliferation in colon cancer cell lines and colonic polyp formation. <italic>Per2</italic> gene activation suppresses tumorigenesis in colon by down-regulation of beta-catenin. Increased beta-catenin affects the circadian clock and enhances PER2 protein degradation in colon cancer. Suppression of human beta-catenin expression inhibits cellular proliferation in intestinal adenomas. Disruption of the peripheral intestinal CRs may contribute to intestinal epithelial neoplastic transformation of human colorectal cancer. The circadian expression of dihydropyrimidine dehydrogenase, an enzyme that is implicated in the metabolism of the anticancer drug 5-fluorouracil, may be regulated by <italic>Per1</italic> in high-grade colon tumors. The ephrin-Eph cell pathway is linked to the Wnt/beta catenin pathway and is involved in colon cancer (Clevers, <xref rid="B24" ref-type="bibr">2006a</xref>,<xref rid="B25" ref-type="bibr">b</xref>).</p><p>Functional bowel disorders are associated with autonomic disturbance (Tougas, <xref rid="B160" ref-type="bibr">2000</xref>). People with type 2 diabetes have an increased risk of developing colorectal cancer. Diabetes is associated with a higher risk of colon cancer (Yuhara et al., <xref rid="B188" ref-type="bibr">2011</xref>). Heart disease increases at twice the risk of bowel cancer. Colon cancer and coronary artery disease are known to share similar risk factors (smoking, high-fat diet, obesity, diabetes, high blood pressure, and sedentary lifestyle) which increase the risk of colon cancer. This suggests that the two diseases may be connected (Chan et al., <xref rid="B21" ref-type="bibr">2007</xref>). People with coronary artery disease are more likely to develop colon cancer than those without.</p></sec></sec></sec><sec><title>Synthesis</title><p>Circadian rhythms (CRs) are particularly fascinating phenomena. They go very far back in evolution. The existence of a CR is the signature of instability. Beyond a point of bifurcation, an unstable thermodynamic system can evolve spontaneously into a periodic state. These periodic oscillations correspond to a phenomenon of self-organization in time and have been called “dissipative structures” (Prigogine et al., <xref rid="B132" ref-type="bibr">1974</xref>). Dissipative structures are far-from-equilibrium systems, such as cyclones, hurricanes, lasers, Bénard cells, Belousov–Zhabotinsky reactions, Turing structures, circadian rhythms, and more generally most of the living organisms. CRs are based on the existence of negative feedback loops. Oscillatory behavior gradually has been integrated into the living world to become one of its major characteristics. In the cardiovascular system, circadian genes show properties of anticipation and this makes it possible to coordinate lipid and carbohydrate metabolism with the cardiovascular function, especially for blood pressure and heart rate. Dysfunction of CRs can be associated with serious clinical problems and may induce a negative impact on quality of life, sometimes with a poor prognosis. Abnormalities of circadian gene function may result in the occurrence of metabolic syndrome, obesity, and even more seriously, stroke, or myocardial infarction.</p><p>Two major systems interfere with circadian genes, namely the canonical Wnt pathway, and the PPAR system. In some cases of diseases presenting profiles 1 or 2, there is not always evidence of the exact influence of CRs on the Wnt-beta catenin-PPAR gamma pathway and cardiac function. PPAR gamma controls the circadian <italic>Clock-Bmal1</italic> genes in the vascular system. Importantly, there is an opposite between activation of the Wnt pathway and PPAR gamma. This is attested by their respective profiles in numerous diseases, either cardiovascular diseases or pathologies with cardiovascular complications. There is a subtle thermodynamic regulation of CRs that run far-from-equilibrium; moreover, there is the need to maintain the balance between the two systems canonical Wnt and PPAR gamma. Indeed, activation of the Wnt system with inactivation of PPAR gamma favors diabetes, hypertension, several cancers, and neurodegenerative diseases. The reverse is observed in ARVD, osteoporosis, Alzheimer disease, bipolar disorder, schizophrenia, and myocardial ischemia. The extreme complexity of the Wnt-PPAR systems and their numerous inter-related pathways partly explain their involvement in numerous diseases. We remain surprised by both the number and the importance of these diseases, causing considerable morbidity, and mortality and heavy social and economic costs.</p><p>The discovery and use of new agonist or antagonist pharmacological agents acting on PPARs, and more generally, directly or indirectly implied in the canonical Wnt system, are particularly important. This leads to numerous novel therapeutic approaches. PPAR gamma is a key regulator of lipid metabolism and its activation by some TZD is used for the treatment of type 2 diabetes and protects against atherosclerosis. However, some TZD have been reported to cause a higher rate of fractures in human patients. Pharmacological inhibition of PPAR gamma represents a potential therapeutic approach for age-related bone loss. Induction of the Wnt pathway or inhibition of Wnt antagonists may offer therapeutic opportunities in treating bone disorders, including osteoporosis. Antibodies targeting the Wnt inhibitor sclerostin lead to increased bone mineral density in post-menopausal women. Lithium, often used to treat bipolar disorder, blocks a Wnt antagonist, decreasing the patient's risk of fractures. Lithium exerts effects on components of the Wnt signaling pathway. The Wnt signaling pathway plays an important role in the treatment of bipolar disorder. The future development of selective GSK3- beta inhibitors may have considerable utility not only for the treatment of bipolar disorder but also for a variety of neurodegenerative disorders. Therapies targeting the Wnt pathway are not without risk, and may lead to over-activation of Wnt/catenin and its association with many tumors. However, it is conceivable that targeting Wnt inhibitors may predispose the individuals to tumorigenic phenotypes.</p><sec><title>Conflict of interest statement</title><p>The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.</p></sec></sec></body><back><ack><p>We would like to thank Mr. Vincent Gobert and Dr. Michel Grivaux, Director of the Clinical Research Center of the Meaux Hospital, France.</p></ack><ref-list><title>References</title><ref id="B1"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Akashi</surname><given-names>M.</given-names></name><name><surname>Takumi</surname><given-names>T.</given-names></name></person-group> (<year>2005</year>). <article-title>The orphan nuclear receptor RORalpha regulates circadian transcription of the mammalian core-clock Bmal1</article-title>. <source>Nat. Struct. Mol. Biol</source>. <volume>12</volume>, <fpage>441</fpage>–<lpage>448</lpage>. <pub-id pub-id-type="doi">10.1038/nsmb925</pub-id><pub-id pub-id-type="pmid">15821743</pub-id></mixed-citation></ref><ref id="B2"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Anan</surname><given-names>F.</given-names></name><name><surname>Masaki</surname><given-names>T.</given-names></name><name><surname>Fukunaga</surname><given-names>N.</given-names></name><name><surname>Teshima</surname><given-names>Y.</given-names></name><name><surname>Iwao</surname><given-names>T.</given-names></name><name><surname>Kaneda</surname><given-names>K.</given-names></name><etal></etal></person-group>. (<year>2007</year>). <article-title>Pioglitazone shift circadian rhythm of blood pressure from non-dipper to dipper type in type 2 diabetes mellitus</article-title>. <source>Eur. J. Clin. Invest</source>. <volume>37</volume>, <fpage>709</fpage>–<lpage>714</lpage>. <pub-id pub-id-type="doi">10.1111/j.1365-2362.2007.01854.x</pub-id><pub-id pub-id-type="pmid">17696960</pub-id></mixed-citation></ref><ref id="B3"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Andreassen</surname><given-names>O. A.</given-names></name><name><surname>Djurovic</surname><given-names>S.</given-names></name><name><surname>Thompson</surname><given-names>W. K.</given-names></name><name><surname>Schork</surname><given-names>A. J.</given-names></name><name><surname>Kendler</surname><given-names>K. S.</given-names></name><name><surname>O'Donovan</surname><given-names>M. C.</given-names></name><etal></etal></person-group>. (<year>2013</year>). <article-title>Improved detection of common variants associated with schizophrenia by leveraging pleiotropy with cardiovascular-disease risk factors</article-title>. <source>Am. J. Hum. Genet</source>. <volume>92</volume>, <fpage>197</fpage>–<lpage>209</lpage>. <pub-id pub-id-type="doi">10.1016/j.ajhg.2013.01.001</pub-id><pub-id pub-id-type="pmid">23375658</pub-id></mixed-citation></ref><ref id="B4"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Andrich</surname><given-names>J.</given-names></name><name><surname>Schmitz</surname><given-names>T.</given-names></name><name><surname>Saft</surname><given-names>C.</given-names></name><name><surname>Postert</surname><given-names>T.</given-names></name><name><surname>Kraus</surname><given-names>P.</given-names></name><name><surname>Epplen</surname><given-names>J. T.</given-names></name><etal></etal></person-group>. (<year>2002</year>). <article-title>Autonomic nervous system function in Huntington's disease</article-title>. <source>J. Neurol. Neurosurg. Psychiatry</source><volume>72</volume>, <fpage>726</fpage>–<lpage>731</lpage>. <pub-id pub-id-type="doi">10.1136/jnnp.72.6.726</pub-id><pub-id pub-id-type="pmid">12023413</pub-id></mixed-citation></ref><ref id="B5"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Anea</surname><given-names>C. B.</given-names></name><name><surname>Zhang</surname><given-names>M.</given-names></name><name><surname>Stepp</surname><given-names>D. W.</given-names></name><name><surname>Simkins</surname><given-names>G. B.</given-names></name><name><surname>Reed</surname><given-names>G.</given-names></name><name><surname>Fulton</surname><given-names>D. J.</given-names></name><etal></etal></person-group>. (<year>2009</year>). <article-title>Vascular disease in mice with a dysfunctional circadian clock</article-title>. <source>Circulation</source><volume>119</volume>, <fpage>1510</fpage>–<lpage>1517</lpage>. <pub-id pub-id-type="doi">10.1161/CIRCULATIONAHA.108.827477</pub-id><pub-id pub-id-type="pmid">19273720</pub-id></mixed-citation></ref><ref id="B6"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Aziz</surname><given-names>N. A.</given-names></name><name><surname>Anguelova</surname><given-names>G. V.</given-names></name><name><surname>Marinus</surname><given-names>J.</given-names></name><name><surname>Lammers</surname><given-names>G. J.</given-names></name><name><surname>Roos</surname><given-names>R. A.</given-names></name></person-group> (<year>2010</year>). <article-title>Sleep and circadian rhythm alterations correlate with depression and cognitive impairment in Huntington's disease</article-title>. <source>Parkinsonism Relat. Disord</source>. <volume>16</volume>, <fpage>345</fpage>–<lpage>350</lpage>. <pub-id pub-id-type="doi">10.1016/j.parkreldis.2010.02.009</pub-id><pub-id pub-id-type="pmid">20236854</pub-id></mixed-citation></ref><ref id="B7"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Barger</surname><given-names>P. M.</given-names></name><name><surname>Brandt</surname><given-names>J. M.</given-names></name><name><surname>Leone</surname><given-names>T. C.</given-names></name><name><surname>Weinheimer</surname><given-names>C. J.</given-names></name><name><surname>Kelly</surname><given-names>D. P.</given-names></name></person-group> (<year>2000</year>). <article-title>Deactivation of peroxisome proliferator-activated receptor-alpha during cardiac hypertrophic growth</article-title>. <source>J. Clin. Invest</source>. <volume>105</volume>, <fpage>1723</fpage>–<lpage>1730</lpage>. <pub-id pub-id-type="doi">10.1172/JCI9056</pub-id><pub-id pub-id-type="pmid">10862787</pub-id></mixed-citation></ref><ref id="B8"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Basso</surname><given-names>C.</given-names></name><name><surname>Corrado</surname><given-names>D.</given-names></name><name><surname>Marcus</surname><given-names>F. I.</given-names></name><name><surname>Nava</surname><given-names>A.</given-names></name><name><surname>Thiene</surname><given-names>G.</given-names></name></person-group> (<year>2009</year>). <article-title>Arrhythmogenic right ventricular cardiomyopathy</article-title>. <source>Lancet</source><volume>373</volume>, <fpage>1289</fpage>–<lpage>1300</lpage>. <pub-id pub-id-type="doi">10.1016/S0140-6736(09)60256-7</pub-id><pub-id pub-id-type="pmid">19362677</pub-id></mixed-citation></ref><ref id="B9"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Belanger</surname><given-names>A. J.</given-names></name><name><surname>Lu</surname><given-names>H.</given-names></name><name><surname>Date</surname><given-names>T.</given-names></name><name><surname>Liu</surname><given-names>L. X.</given-names></name><name><surname>Vincent</surname><given-names>K. A.</given-names></name><name><surname>Akita</surname><given-names>G. Y.</given-names></name><etal></etal></person-group>. (<year>2002</year>). <article-title>Hypoxia up-regulates expression of peroxisome proliferator-activated receptor gamma angiopoietin-related gene (PGAR) in cardiomyocytes: role of hypoxia inducible factor 1alpha</article-title>. <source>J. Mol. Cell. Cardiol</source>. <volume>34</volume>, <fpage>765</fpage>–<lpage>774</lpage>. <pub-id pub-id-type="doi">10.1006/jmcc.2002.2021</pub-id><pub-id pub-id-type="pmid">12099716</pub-id></mixed-citation></ref><ref id="B10"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Benedusi</surname><given-names>V.</given-names></name><name><surname>Martorana</surname><given-names>F.</given-names></name><name><surname>Brambilla</surname><given-names>L.</given-names></name><name><surname>Maggi</surname><given-names>A.</given-names></name><name><surname>Rossi</surname><given-names>D.</given-names></name></person-group> (<year>2012</year>). <article-title>The peroxisome proliferator-activated receptor gamma (PPARgamma) controls natural protective mechanisms against lipid peroxidation in amyotrophic lateral sclerosis</article-title>. <source>J. Biol. Chem</source>. <volume>287</volume>, <fpage>35899</fpage>–<lpage>35911</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.M112.366419</pub-id><pub-id pub-id-type="pmid">22910911</pub-id></mixed-citation></ref><ref id="B11"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ben-Ze'ev</surname><given-names>A.</given-names></name><name><surname>Geiger</surname><given-names>B.</given-names></name></person-group> (<year>1998</year>). <article-title>Differential molecular interactions of beta-catenin and plakoglobin in adhesion, signaling and cancer</article-title>. <source>Curr. Opin. Cell Biol</source>. <volume>10</volume>, <fpage>629</fpage>–<lpage>639</lpage>. <pub-id pub-id-type="doi">10.1016/S0955-0674(98)80039-2</pub-id><pub-id pub-id-type="pmid">9818174</pub-id></mixed-citation></ref><ref id="B12"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Berger</surname><given-names>J.</given-names></name><name><surname>Moller</surname><given-names>D. E.</given-names></name></person-group> (<year>2002</year>). <article-title>The mechanisms of action of PPARs</article-title>. <source>Annu. Rev. Med</source>. <volume>53</volume>, <fpage>409</fpage>–<lpage>435</lpage>. <pub-id pub-id-type="doi">10.1146/annurev.med.53.082901.104018</pub-id><pub-id pub-id-type="pmid">11818483</pub-id></mixed-citation></ref><ref id="B13"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Boonen</surname><given-names>R. A.</given-names></name><name><surname>van Tijn</surname><given-names>P.</given-names></name><name><surname>Zivkovic</surname><given-names>D.</given-names></name></person-group> (<year>2009</year>). <article-title>Wnt signaling in Alzheimer's disease: up or down, that is the question</article-title>. <source>Ageing Res. Rev</source>. <volume>8</volume>, <fpage>71</fpage>–<lpage>82</lpage>. <pub-id pub-id-type="doi">10.1016/j.arr.2008.11.003</pub-id><pub-id pub-id-type="pmid">19101658</pub-id></mixed-citation></ref><ref id="B14"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Brack</surname><given-names>A. S.</given-names></name><name><surname>Conboy</surname><given-names>M. J.</given-names></name><name><surname>Roy</surname><given-names>S.</given-names></name><name><surname>Lee</surname><given-names>M.</given-names></name><name><surname>Kuo</surname><given-names>C. J.</given-names></name><name><surname>Keller</surname><given-names>C.</given-names></name><etal></etal></person-group>. (<year>2007</year>). <article-title>Increased Wnt signaling during aging alters muscle stem cell fate and increases fibrosis</article-title>. <source>Science</source><volume>317</volume>, <fpage>807</fpage>–<lpage>810</lpage>. <pub-id pub-id-type="doi">10.1126/science.1144090</pub-id><pub-id pub-id-type="pmid">17690295</pub-id></mixed-citation></ref><ref id="B15"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bray</surname><given-names>M. S.</given-names></name><name><surname>Shaw</surname><given-names>C. A.</given-names></name><name><surname>Moore</surname><given-names>M. W.</given-names></name><name><surname>Garcia</surname><given-names>R. A.</given-names></name><name><surname>Zanquetta</surname><given-names>M. M.</given-names></name><name><surname>Durgan</surname><given-names>D. J.</given-names></name><etal></etal></person-group>. (<year>2008</year>). <article-title>Disruption of the circadian clock within the cardiomyocyte influences myocardial contractile function, metabolism, and gene expression</article-title>. <source>Am. J. Physiol. Heart. Circ. Physiol</source>. <volume>294</volume>, <fpage>H1036</fpage>–<lpage>H1047</lpage>. <pub-id pub-id-type="doi">10.1152/ajpheart.01291.2007</pub-id><pub-id pub-id-type="pmid">18156197</pub-id></mixed-citation></ref><ref id="B16"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Breen</surname><given-names>D. P.</given-names></name><name><surname>Vuono</surname><given-names>R.</given-names></name><name><surname>Nawarathna</surname><given-names>U.</given-names></name><name><surname>Fisher</surname><given-names>K.</given-names></name><name><surname>Shneerson</surname><given-names>J. M.</given-names></name><name><surname>Reddy</surname><given-names>A. B.</given-names></name><etal></etal></person-group>. (<year>2014</year>). <article-title>Sleep and circadian rhythm regulation in early Parkinson disease</article-title>. <source>JAMA Neurol</source>. <volume>71</volume>, <fpage>589</fpage>–<lpage>595</lpage>. <pub-id pub-id-type="doi">10.1001/jamaneurol.2014.65</pub-id><pub-id pub-id-type="pmid">24687146</pub-id></mixed-citation></ref><ref id="B17"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cai</surname><given-names>Y.</given-names></name><name><surname>Liu</surname><given-names>S.</given-names></name><name><surname>Sothern</surname><given-names>R. B.</given-names></name><name><surname>Xu</surname><given-names>S.</given-names></name><name><surname>Chan</surname><given-names>P.</given-names></name></person-group> (<year>2010</year>). <article-title>Expression of clock genes Per1 and Bmal1 in total leukocytes in health and Parkinson's disease</article-title>. <source>Eur. J. Neurol</source>. <volume>17</volume>, <fpage>550</fpage>–<lpage>554</lpage>. <pub-id pub-id-type="doi">10.1111/j.1468-1331.2009.02848.x</pub-id><pub-id pub-id-type="pmid">19912323</pub-id></mixed-citation></ref><ref id="B18"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Canalis</surname><given-names>E.</given-names></name></person-group> (<year>2013</year>). <article-title>Wnt signalling in osteoporosis: mechanisms and novel therapeutic approaches</article-title>. <source>Nat. Rev. Endocrinol</source>. <volume>9</volume>, <fpage>575</fpage>–<lpage>583</lpage>. <pub-id pub-id-type="doi">10.1038/nrendo.2013.154</pub-id><pub-id pub-id-type="pmid">23938284</pub-id></mixed-citation></ref><ref id="B19"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Canaple</surname><given-names>L.</given-names></name><name><surname>Rambaud</surname><given-names>J.</given-names></name><name><surname>Dkhissi-Benyahya</surname><given-names>O.</given-names></name><name><surname>Rayet</surname><given-names>B.</given-names></name><name><surname>Tan</surname><given-names>N. S.</given-names></name><name><surname>Michalik</surname><given-names>L.</given-names></name><etal></etal></person-group>. (<year>2006</year>). <article-title>Reciprocal regulation of brain and muscle Arnt-like protein 1 and peroxisome proliferator-activated receptor alpha defines a novel positive feedback loop in the rodent liver circadian clock</article-title>. <source>Mol. Endocrinol</source>. <volume>20</volume>, <fpage>1715</fpage>–<lpage>1727</lpage>. <pub-id pub-id-type="doi">10.1210/me.2006-0052</pub-id><pub-id pub-id-type="pmid">16556735</pub-id></mixed-citation></ref><ref id="B20"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cermakian</surname><given-names>N.</given-names></name><name><surname>Lamont</surname><given-names>E. W.</given-names></name><name><surname>Boudreau</surname><given-names>P.</given-names></name><name><surname>Boivin</surname><given-names>D. B.</given-names></name></person-group> (<year>2011</year>). <article-title>Circadian clock gene expression in brain regions of Alzheimer's disease patients and control subjects</article-title>. <source>J. Biol. Rhythms</source><volume>26</volume>, <fpage>160</fpage>–<lpage>170</lpage>. <pub-id pub-id-type="doi">10.1177/0748730410395732</pub-id><pub-id pub-id-type="pmid">21454296</pub-id></mixed-citation></ref><ref id="B21"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chan</surname><given-names>A. O.</given-names></name><name><surname>Jim</surname><given-names>M. H.</given-names></name><name><surname>Lam</surname><given-names>K. F.</given-names></name><name><surname>Morris</surname><given-names>J. S.</given-names></name><name><surname>Siu</surname><given-names>D. C.</given-names></name><name><surname>Tong</surname><given-names>T.</given-names></name><etal></etal></person-group>. (<year>2007</year>). <article-title>Prevalence of colorectal neoplasm among patients with newly diagnosed coronary artery disease</article-title>. <source>JAMA</source><volume>298</volume>, <fpage>1412</fpage>–<lpage>1419</lpage>. <pub-id pub-id-type="doi">10.1001/jama.298.12.1412</pub-id><pub-id pub-id-type="pmid">17895457</pub-id></mixed-citation></ref><ref id="B22"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chatterjee</surname><given-names>S.</given-names></name><name><surname>Nam</surname><given-names>D.</given-names></name><name><surname>Guo</surname><given-names>B.</given-names></name><name><surname>Kim</surname><given-names>J. M.</given-names></name><name><surname>Winnier</surname><given-names>G. E.</given-names></name><name><surname>Lee</surname><given-names>J.</given-names></name><etal></etal></person-group>. (<year>2013</year>). <article-title>Brain and muscle Arnt-like 1 is a key regulator of myogenesis</article-title>. <source>J. Cell Sci</source>. <volume>126</volume>, <fpage>2213</fpage>–<lpage>2224</lpage>. <pub-id pub-id-type="doi">10.1242/jcs.120519</pub-id><pub-id pub-id-type="pmid">23525013</pub-id></mixed-citation></ref><ref id="B23"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chen</surname><given-names>L.</given-names></name><name><surname>Yang</surname><given-names>G.</given-names></name></person-group> (<year>2014</year>). <article-title>PPARs integrate the mammalian clock and energy metabolism</article-title>. <source>PPAR Res</source>. <volume>2014</volume>:<fpage>653017</fpage>. <pub-id pub-id-type="doi">10.1155/2014/653017</pub-id><pub-id pub-id-type="pmid">24693278</pub-id></mixed-citation></ref><ref id="B24"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Clevers</surname><given-names>H.</given-names></name></person-group> (<year>2006a</year>). <article-title>Colon cancer–understanding how NSAIDs work</article-title>. <source>N. Engl. J. Med</source>. <volume>354</volume>, <fpage>761</fpage>–<lpage>763</lpage>. <pub-id pub-id-type="doi">10.1056/NEJMcibr055457</pub-id><pub-id pub-id-type="pmid">16481647</pub-id></mixed-citation></ref><ref id="B25"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Clevers</surname><given-names>H.</given-names></name></person-group> (<year>2006b</year>). <article-title>Wnt/beta-catenin signaling in development and disease</article-title>. <source>Cell</source><volume>127</volume>, <fpage>469</fpage>–<lpage>480</lpage>. <pub-id pub-id-type="doi">10.1016/j.cell.2006.10.018</pub-id><pub-id pub-id-type="pmid">17081971</pub-id></mixed-citation></ref><ref id="B26"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Clevers</surname><given-names>H.</given-names></name><name><surname>Batlle</surname><given-names>E.</given-names></name></person-group> (<year>2006</year>). <article-title>EphB/EphrinB receptors and Wnt signaling in colorectal cancer</article-title>. <source>Cancer Res</source>. <volume>66</volume>, <fpage>2</fpage>–<lpage>5</lpage>. <pub-id pub-id-type="doi">10.1158/0008-5472.CAN-05-3849</pub-id><pub-id pub-id-type="pmid">16397205</pub-id></mixed-citation></ref><ref id="B27"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Coppola</surname><given-names>G.</given-names></name><name><surname>Marmolino</surname><given-names>D.</given-names></name><name><surname>Lu</surname><given-names>D.</given-names></name><name><surname>Wang</surname><given-names>Q.</given-names></name><name><surname>Cnop</surname><given-names>M.</given-names></name><name><surname>Rai</surname><given-names>M.</given-names></name><etal></etal></person-group>. (<year>2009</year>). <article-title>Functional genomic analysis of frataxin deficiency reveals tissue-specific alterations and identifies the PPARgamma pathway as a therapeutic target in Friedreich's ataxia</article-title>. <source>Hum. Mol. Genet</source>. <volume>18</volume>, <fpage>2452</fpage>–<lpage>2461</lpage>. <pub-id pub-id-type="doi">10.1093/hmg/ddp183</pub-id><pub-id pub-id-type="pmid">19376812</pub-id></mixed-citation></ref><ref id="B28"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Corrado</surname><given-names>D.</given-names></name><name><surname>Basso</surname><given-names>C.</given-names></name><name><surname>Thiene</surname><given-names>G.</given-names></name><name><surname>McKenna</surname><given-names>W. J.</given-names></name><name><surname>Davies</surname><given-names>M. J.</given-names></name><name><surname>Fontaliran</surname><given-names>F.</given-names></name><etal></etal></person-group>. (<year>1997</year>). <article-title>Spectrum of clinicopathologic manifestations of arrhythmogenic right ventricular cardiomyopathy/dysplasia: a multicenter study</article-title>. <source>J. Am. Coll. Cardiol</source>. <volume>30</volume>, <fpage>1512</fpage>–<lpage>1520</lpage>. <pub-id pub-id-type="doi">10.1016/S0735-1097(97)00332-X</pub-id><pub-id pub-id-type="pmid">9362410</pub-id></mixed-citation></ref><ref id="B29"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Curtis</surname><given-names>A. M.</given-names></name><name><surname>Cheng</surname><given-names>Y.</given-names></name><name><surname>Kapoor</surname><given-names>S.</given-names></name><name><surname>Reilly</surname><given-names>D.</given-names></name><name><surname>Price</surname><given-names>T. S.</given-names></name><name><surname>Fitzgerald</surname><given-names>G. A.</given-names></name></person-group> (<year>2007</year>). <article-title>Circadian variation of blood pressure and the vascular response to asynchronous stress</article-title>. <source>Proc. Natl. Acad. Sci. U.S.A</source>. <volume>104</volume>, <fpage>3450</fpage>–<lpage>3455</lpage>. <pub-id pub-id-type="doi">10.1073/pnas.0611680104</pub-id><pub-id pub-id-type="pmid">17360665</pub-id></mixed-citation></ref><ref id="B30"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>De Ferrari</surname><given-names>G.</given-names></name><name><surname>Avila</surname><given-names>M.</given-names></name><name><surname>Medina</surname><given-names>M.</given-names></name><name><surname>Perez-Palma</surname><given-names>E.</given-names></name><name><surname>Bustos</surname><given-names>B.</given-names></name><name><surname>Alarcon</surname><given-names>M.</given-names></name></person-group> (<year>2014</year>). <article-title>Wnt/beta-Catenin Signaling in Alzheimer's Disease</article-title>. <source>CNS Neurol. Disord. Drug Targets</source><volume>13</volume>, <fpage>745</fpage>–<lpage>754</lpage>. <pub-id pub-id-type="pmid">24365184</pub-id></mixed-citation></ref><ref id="B31"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Desjardins</surname><given-names>F.</given-names></name><name><surname>Sekkali</surname><given-names>B.</given-names></name><name><surname>Verreth</surname><given-names>W.</given-names></name><name><surname>Pelat</surname><given-names>M.</given-names></name><name><surname>De Keyzer</surname><given-names>D.</given-names></name><name><surname>Mertens</surname><given-names>A.</given-names></name><etal></etal></person-group>. (<year>2008</year>). <article-title>Rosuvastatin increases vascular endothelial PPARgamma expression and corrects blood pressure variability in obese dyslipidaemic mice</article-title>. <source>Eur. Heart J</source>. <volume>29</volume>, <fpage>128</fpage>–<lpage>137</lpage>. <pub-id pub-id-type="doi">10.1093/eurheartj/ehm540</pub-id><pub-id pub-id-type="pmid">18063594</pub-id></mixed-citation></ref><ref id="B32"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Djouadi</surname><given-names>F.</given-names></name><name><surname>Lecarpentier</surname><given-names>Y.</given-names></name><name><surname>Hebert</surname><given-names>J. L.</given-names></name><name><surname>Charron</surname><given-names>P.</given-names></name><name><surname>Bastin</surname><given-names>J.</given-names></name><name><surname>Coirault</surname><given-names>C.</given-names></name></person-group> (<year>2009</year>). <article-title>A potential link between PPAR signaling and the pathogenesis of arrhythmogenic right ventricular cardiomyopathy (ARVC)</article-title>. <source>Cardiovasc. Res</source>. <volume>84</volume>, <fpage>83</fpage>–<lpage>90</lpage>. <pub-id pub-id-type="doi">10.1093/cvr/cvp183</pub-id><pub-id pub-id-type="pmid">19497962</pub-id></mixed-citation></ref><ref id="B33"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Drew</surname><given-names>P. D.</given-names></name><name><surname>Xu</surname><given-names>J.</given-names></name><name><surname>Racke</surname><given-names>M. K.</given-names></name></person-group> (<year>2008</year>). <article-title>PPAR-gamma: therapeutic potential for multiple sclerosis</article-title>. <source>PPAR Res</source>. <volume>2008</volume>:<fpage>627463</fpage>. <pub-id pub-id-type="doi">10.1155/2008/627463</pub-id><pub-id pub-id-type="pmid">18604287</pub-id></mixed-citation></ref><ref id="B34"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Druschky</surname><given-names>A.</given-names></name><name><surname>Spitzer</surname><given-names>A.</given-names></name><name><surname>Platsch</surname><given-names>G.</given-names></name><name><surname>Claus</surname><given-names>D.</given-names></name><name><surname>Feistel</surname><given-names>H.</given-names></name><name><surname>Druschky</surname><given-names>K.</given-names></name><etal></etal></person-group>. (<year>1999</year>). <article-title>Cardiac sympathetic denervation in early stages of amyotrophic lateral sclerosis demonstrated by 123I-MIBG-SPECT</article-title>. <source>Acta Neurol. Scand</source>. <volume>99</volume>, <fpage>308</fpage>–<lpage>314</lpage>. <pub-id pub-id-type="doi">10.1111/j.1600-0404.1999.tb00681.x</pub-id><pub-id pub-id-type="pmid">10348161</pub-id></mixed-citation></ref><ref id="B35"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dupont</surname><given-names>P.</given-names></name><name><surname>Besson</surname><given-names>M. T.</given-names></name><name><surname>Devaux</surname><given-names>J.</given-names></name><name><surname>Lievens</surname><given-names>J. C.</given-names></name></person-group> (<year>2012</year>). <article-title>Reducing canonical Wingless/Wnt signaling pathway confers protection against mutant Huntingtin toxicity in Drosophila</article-title>. <source>Neurobiol. Dis</source>. <volume>47</volume>, <fpage>237</fpage>–<lpage>247</lpage>. <pub-id pub-id-type="doi">10.1016/j.nbd.2012.04.007</pub-id><pub-id pub-id-type="pmid">22531500</pub-id></mixed-citation></ref><ref id="B36"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Duque</surname><given-names>G.</given-names></name><name><surname>Li</surname><given-names>W.</given-names></name><name><surname>Vidal</surname><given-names>C.</given-names></name><name><surname>Bermeo</surname><given-names>S.</given-names></name><name><surname>Rivas</surname><given-names>D.</given-names></name><name><surname>Henderson</surname><given-names>J.</given-names></name></person-group> (<year>2013</year>). <article-title>Pharmacological inhibition of PPARgamma increases osteoblastogenesis and bone mass in male C57BL/6 mice</article-title>. <source>J. Bone Miner. Res</source>. <volume>28</volume>, <fpage>639</fpage>–<lpage>648</lpage>. <pub-id pub-id-type="doi">10.1002/jbmr.1782</pub-id><pub-id pub-id-type="pmid">23044841</pub-id></mixed-citation></ref><ref id="B37"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Durgan</surname><given-names>D. J.</given-names></name><name><surname>Hotze</surname><given-names>M. A.</given-names></name><name><surname>Tomlin</surname><given-names>T. M.</given-names></name><name><surname>Egbejimi</surname><given-names>O.</given-names></name><name><surname>Graveleau</surname><given-names>C.</given-names></name><name><surname>Abel</surname><given-names>E. D.</given-names></name><etal></etal></person-group>. (<year>2005</year>). <article-title>The intrinsic circadian clock within the cardiomyocyte</article-title>. <source>Am. J. Physiol. Heart Circ. Physiol</source>. <volume>289</volume>, <fpage>H1530</fpage>–<lpage>H1541</lpage>. <pub-id pub-id-type="doi">10.1152/ajpheart.00406.2005</pub-id><pub-id pub-id-type="pmid">15937094</pub-id></mixed-citation></ref><ref id="B38"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Durgan</surname><given-names>D. J.</given-names></name><name><surname>Moore</surname><given-names>M. W.</given-names></name><name><surname>Ha</surname><given-names>N. P.</given-names></name><name><surname>Egbejimi</surname><given-names>O.</given-names></name><name><surname>Fields</surname><given-names>A.</given-names></name><name><surname>Mbawuike</surname><given-names>U.</given-names></name><etal></etal></person-group>. (<year>2007</year>). <article-title>Circadian rhythms in myocardial metabolism and contractile function: influence of workload and oleate</article-title>. <source>Am. J. Physiol. Heart Circ. Physiol</source>. <volume>293</volume>, <fpage>H2385</fpage>–<lpage>H2393</lpage>. <pub-id pub-id-type="doi">10.1152/ajpheart.01361.2006</pub-id><pub-id pub-id-type="pmid">17616739</pub-id></mixed-citation></ref><ref id="B39"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Durgan</surname><given-names>D. J.</given-names></name><name><surname>Trexler</surname><given-names>N. A.</given-names></name><name><surname>Egbejimi</surname><given-names>O.</given-names></name><name><surname>McElfresh</surname><given-names>T. A.</given-names></name><name><surname>Suk</surname><given-names>H. Y.</given-names></name><name><surname>Petterson</surname><given-names>L. E.</given-names></name><etal></etal></person-group>. (<year>2006</year>). <article-title>The circadian clock within the cardiomyocyte is essential for responsiveness of the heart to fatty acids</article-title>. <source>J. Biol. Chem</source>. <volume>281</volume>, <fpage>24254</fpage>–<lpage>24269</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.M601704200</pub-id><pub-id pub-id-type="pmid">16798731</pub-id></mixed-citation></ref><ref id="B40"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Edery</surname><given-names>I.</given-names></name></person-group> (<year>2000</year>). <article-title>Circadian rhythms in a nutshell</article-title>. <source>Physiol Genomics</source><volume>3</volume>, <fpage>59</fpage>–<lpage>74</lpage>. <pub-id pub-id-type="pmid">11015601</pub-id></mixed-citation></ref><ref id="B41"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Farhat</surname><given-names>G. N.</given-names></name><name><surname>Cauley</surname><given-names>J. A.</given-names></name></person-group> (<year>2008</year>). <article-title>The link between osteoporosis and cardiovascular disease</article-title>. <source>Clin. Cases Miner. Bone Metab</source>. <volume>5</volume>, <fpage>19</fpage>–<lpage>34</lpage>. <pub-id pub-id-type="pmid">22460842</pub-id></mixed-citation></ref><ref id="B42"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Finck</surname><given-names>B. N.</given-names></name><name><surname>Bernal-Mizrachi</surname><given-names>C.</given-names></name><name><surname>Han</surname><given-names>D. H.</given-names></name><name><surname>Coleman</surname><given-names>T.</given-names></name><name><surname>Sambandam</surname><given-names>N.</given-names></name><name><surname>LaRiviere</surname><given-names>L. L.</given-names></name><etal></etal></person-group>. (<year>2005</year>). <article-title>A potential link between muscle peroxisome proliferator- activated receptor-alpha signaling and obesity-related diabetes</article-title>. <source>Cell Metab</source>. <volume>1</volume>, <fpage>133</fpage>–<lpage>144</lpage>. <pub-id pub-id-type="doi">10.1016/j.cmet.2005.01.006</pub-id><pub-id pub-id-type="pmid">16054054</pub-id></mixed-citation></ref><ref id="B43"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Finck</surname><given-names>B. N.</given-names></name><name><surname>Kelly</surname><given-names>D. P.</given-names></name></person-group> (<year>2002</year>). <article-title>Peroxisome proliferator-activated receptor alpha (PPARalpha) signaling in the gene regulatory control of energy metabolism in the normal and diseased heart</article-title>. <source>J. Mol. Cell. Cardiol</source>. <volume>34</volume>, <fpage>1249</fpage>–<lpage>1257</lpage>. <pub-id pub-id-type="doi">10.1006/jmcc.2002.2061</pub-id><pub-id pub-id-type="pmid">12425323</pub-id></mixed-citation></ref><ref id="B44"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Finck</surname><given-names>B. N.</given-names></name><name><surname>Lehman</surname><given-names>J. J.</given-names></name><name><surname>Leone</surname><given-names>T. C.</given-names></name><name><surname>Welch</surname><given-names>M. J.</given-names></name><name><surname>Bennett</surname><given-names>M. J.</given-names></name><name><surname>Kovacs</surname><given-names>A.</given-names></name><etal></etal></person-group>. (<year>2002</year>). <article-title>The cardiac phenotype induced by PPARalpha overexpression mimics that caused by diabetes mellitus</article-title>. <source>J. Clin. Invest</source>. <volume>109</volume>, <fpage>121</fpage>–<lpage>130</lpage>. <pub-id pub-id-type="doi">10.1172/JCI0214080</pub-id><pub-id pub-id-type="pmid">11781357</pub-id></mixed-citation></ref><ref id="B45"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Fontaine</surname><given-names>C.</given-names></name><name><surname>Dubois</surname><given-names>G.</given-names></name><name><surname>Duguay</surname><given-names>Y.</given-names></name><name><surname>Helledie</surname><given-names>T.</given-names></name><name><surname>Vu-Dac</surname><given-names>N.</given-names></name><name><surname>Gervois</surname><given-names>P.</given-names></name><etal></etal></person-group>. (<year>2003</year>). <article-title>The orphan nuclear receptor Rev-Erbalpha is a peroxisome proliferator-activated receptor (PPAR) gamma target gene and promotes PPARgamma-induced adipocyte differentiation</article-title>. <source>J. Biol. Chem</source>. <volume>278</volume>, <fpage>37672</fpage>–<lpage>37680</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.M304664200</pub-id><pub-id pub-id-type="pmid">12821652</pub-id></mixed-citation></ref><ref id="B46"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Fontaine</surname><given-names>G.</given-names></name><name><surname>Fontaliran</surname><given-names>F.</given-names></name><name><surname>Hebert</surname><given-names>J. L.</given-names></name><name><surname>Chemla</surname><given-names>D.</given-names></name><name><surname>Zenati</surname><given-names>O.</given-names></name><name><surname>Lecarpentier</surname><given-names>Y.</given-names></name><etal></etal></person-group>. (<year>1999</year>). <article-title>Arrhythmogenic right ventricular dysplasia</article-title>. <source>Annu. Rev. Med</source>. <volume>50</volume>, <fpage>17</fpage>–<lpage>35</lpage>. <pub-id pub-id-type="doi">10.1146/annurev.med.50.1.17</pub-id><pub-id pub-id-type="pmid">10073261</pub-id></mixed-citation></ref><ref id="B47"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Fressard</surname><given-names>V.</given-names></name><name><surname>Duthoit</surname><given-names>G.</given-names></name><name><surname>Donal</surname><given-names>E.</given-names></name><name><surname>Probst</surname><given-names>V.</given-names></name><name><surname>Deharo</surname><given-names>J.-C.</given-names></name><name><surname>Chevalier</surname><given-names>P.</given-names></name><etal></etal></person-group>. (<year>2010</year>). <article-title>Desmosomal genes analysis in arrhythmogenic right ventricular dysplasia/cardiomyopathy: spectrum of mutations and clinical impact in practice</article-title>. <source>Europace</source><volume>12</volume>, <fpage>861</fpage>–<lpage>868</lpage>. <pub-id pub-id-type="doi">10.1093/europace/euq104</pub-id><pub-id pub-id-type="pmid">20400443</pub-id></mixed-citation></ref><ref id="B48"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Galli</surname><given-names>C.</given-names></name><name><surname>Piemontese</surname><given-names>M.</given-names></name><name><surname>Lumetti</surname><given-names>S.</given-names></name><name><surname>Manfredi</surname><given-names>E.</given-names></name><name><surname>Macaluso</surname><given-names>G. M.</given-names></name><name><surname>Passeri</surname><given-names>G.</given-names></name></person-group> (<year>2013</year>). <article-title>GSK3b-inhibitor lithium chloride enhances activation of Wnt canonical signaling and osteoblast differentiation on hydrophilic titanium surfaces</article-title>. <source>Clin. Oral Implants Res</source>. <volume>24</volume>, <fpage>921</fpage>–<lpage>927</lpage>. <pub-id pub-id-type="doi">10.1111/j.1600-0501.2012.02488.x</pub-id><pub-id pub-id-type="pmid">22626030</pub-id></mixed-citation></ref><ref id="B49"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Garcia-Gras</surname><given-names>E.</given-names></name><name><surname>Lombardi</surname><given-names>R.</given-names></name><name><surname>Giocondo</surname><given-names>M. J.</given-names></name><name><surname>Willerson</surname><given-names>J. T.</given-names></name><name><surname>Schneider</surname><given-names>M. D.</given-names></name><name><surname>Khoury</surname><given-names>D. S.</given-names></name><etal></etal></person-group>. (<year>2006</year>). <article-title>Suppression of canonical Wnt/beta-catenin signaling by nuclear plakoglobin recapitulates phenotype of arrhythmogenic right ventricular cardiomyopathy</article-title>. <source>J. Clin. Invest</source>. <volume>116</volume>, <fpage>2012</fpage>–<lpage>2021</lpage>. <pub-id pub-id-type="doi">10.1172/JCI27751</pub-id><pub-id pub-id-type="pmid">16823493</pub-id></mixed-citation></ref><ref id="B50"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gdynia</surname><given-names>H. J.</given-names></name><name><surname>Kurt</surname><given-names>A.</given-names></name><name><surname>Endruhn</surname><given-names>S.</given-names></name><name><surname>Ludolph</surname><given-names>A. C.</given-names></name><name><surname>Sperfeld</surname><given-names>A. D.</given-names></name></person-group> (<year>2006</year>). <article-title>Cardiomyopathy in motor neuron diseases</article-title>. <source>J. Neurol. Neurosurg. Psychiatry</source><volume>77</volume>, <fpage>671</fpage>–<lpage>673</lpage>. <pub-id pub-id-type="doi">10.1136/jnnp.2005.078600</pub-id><pub-id pub-id-type="pmid">16614031</pub-id></mixed-citation></ref><ref id="B51"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gekakis</surname><given-names>N.</given-names></name><name><surname>Staknis</surname><given-names>D.</given-names></name><name><surname>Nguyen</surname><given-names>H. B.</given-names></name><name><surname>Davis</surname><given-names>F. C.</given-names></name><name><surname>Wilsbacher</surname><given-names>L. D.</given-names></name><name><surname>King</surname><given-names>D. P.</given-names></name><etal></etal></person-group>. (<year>1998</year>). <article-title>Role of the CLOCK protein in the mammalian circadian mechanism</article-title>. <source>Science</source><volume>280</volume>, <fpage>1564</fpage>–<lpage>1569</lpage>. <pub-id pub-id-type="doi">10.1126/science.280.5369.1564</pub-id><pub-id pub-id-type="pmid">9616112</pub-id></mixed-citation></ref><ref id="B52"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gervois</surname><given-names>P.</given-names></name><name><surname>Chopin-Delannoy</surname><given-names>S.</given-names></name><name><surname>Fadel</surname><given-names>A.</given-names></name><name><surname>Dubois</surname><given-names>G.</given-names></name><name><surname>Kosykh</surname><given-names>V.</given-names></name><name><surname>Fruchart</surname><given-names>J. C.</given-names></name><etal></etal></person-group>. (<year>1999</year>). <article-title>Fibrates increase human REV-ERBalpha expression in liver via a novel peroxisome proliferator-activated receptor response element</article-title>. <source>Mol. Endocrinol</source>. <volume>13</volume>, <fpage>400</fpage>–<lpage>409</lpage>. <pub-id pub-id-type="pmid">10076997</pub-id></mixed-citation></ref><ref id="B53"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gibbons</surname><given-names>G. F.</given-names></name><name><surname>Patel</surname><given-names>D.</given-names></name><name><surname>Wiggins</surname><given-names>D.</given-names></name><name><surname>Knight</surname><given-names>B. L.</given-names></name></person-group> (<year>2002</year>). <article-title>The functional efficiency of lipogenic and cholesterogenic gene expression in normal mice and in mice lacking the peroxisomal proliferator-activated receptor-alpha (PPAR-alpha)</article-title>. <source>Adv. Enzyme Regul</source>. <volume>42</volume>, <fpage>227</fpage>–<lpage>247</lpage>. <pub-id pub-id-type="doi">10.1016/S0065-2571(01)00033-4</pub-id><pub-id pub-id-type="pmid">12123718</pub-id></mixed-citation></ref><ref id="B54"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Godin</surname><given-names>J. D.</given-names></name><name><surname>Poizat</surname><given-names>G.</given-names></name><name><surname>Hickey</surname><given-names>M. A.</given-names></name><name><surname>Maschat</surname><given-names>F.</given-names></name><name><surname>Humbert</surname><given-names>S.</given-names></name></person-group> (<year>2010</year>). <article-title>Mutant huntingtin-impaired degradation of beta-catenin causes neurotoxicity in Huntington's disease</article-title>. <source>EMBO J</source>. <volume>29</volume>, <fpage>2433</fpage>–<lpage>2445</lpage>. <pub-id pub-id-type="doi">10.1038/emboj.2010.117</pub-id><pub-id pub-id-type="pmid">20531388</pub-id></mixed-citation></ref><ref id="B55"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Goldbeter</surname><given-names>A.</given-names></name></person-group> (<year>2002</year>). <article-title>Computational approaches to cellular rhythms</article-title>. <source>Nature</source><volume>420</volume>, <fpage>238</fpage>–<lpage>245</lpage>. <pub-id pub-id-type="doi">10.1038/nature01259</pub-id><pub-id pub-id-type="pmid">12432409</pub-id></mixed-citation></ref><ref id="B56"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Goldbeter</surname><given-names>A.</given-names></name></person-group> (<year>2013</year>). <article-title>Origin of cyclicity in bipolar disorders: a computational approach</article-title>. <source>Pharmacopsychiatry</source><volume>46</volume>(<issue>Suppl. 1</issue>), <fpage>S44</fpage>–<lpage>S52</lpage>. <pub-id pub-id-type="doi">10.1055/s-0033-1341502</pub-id><pub-id pub-id-type="pmid">23599245</pub-id></mixed-citation></ref><ref id="B57"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Goodwin</surname><given-names>B. C.</given-names></name></person-group> (<year>1965</year>). <article-title>Oscillatory behavior in enzymatic control processes</article-title>. <source>Adv. Enzyme Regul</source>. <volume>3</volume>, <fpage>425</fpage>–<lpage>438</lpage>. <pub-id pub-id-type="doi">10.1016/0065-2571(65)90067-1</pub-id><pub-id pub-id-type="pmid">5861813</pub-id></mixed-citation></ref><ref id="B58"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gould</surname><given-names>T. D.</given-names></name><name><surname>Manji</surname><given-names>H. K.</given-names></name></person-group> (<year>2002</year>). <article-title>The Wnt signaling pathway in bipolar disorder</article-title>. <source>Neuroscientist</source><volume>8</volume>, <fpage>497</fpage>–<lpage>511</lpage>. <pub-id pub-id-type="doi">10.1177/107385802237176</pub-id><pub-id pub-id-type="pmid">12374432</pub-id></mixed-citation></ref><ref id="B59"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Green</surname><given-names>C. B.</given-names></name><name><surname>Douris</surname><given-names>N.</given-names></name><name><surname>Kojima</surname><given-names>S.</given-names></name><name><surname>Strayer</surname><given-names>C. A.</given-names></name><name><surname>Fogerty</surname><given-names>J.</given-names></name><name><surname>Lourim</surname><given-names>D.</given-names></name><etal></etal></person-group>. (<year>2007</year>). <article-title>Loss of Nocturnin, a circadian deadenylase, confers resistance to hepatic steatosis and diet-induced obesity</article-title>. <source>Proc. Natl. Acad. Sci. U.S.A</source>. <volume>104</volume>, <fpage>9888</fpage>–<lpage>9893</lpage>. <pub-id pub-id-type="doi">10.1073/pnas.0702448104</pub-id><pub-id pub-id-type="pmid">17517647</pub-id></mixed-citation></ref><ref id="B60"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Guo</surname><given-names>B.</given-names></name><name><surname>Chatterjee</surname><given-names>S.</given-names></name><name><surname>Li</surname><given-names>L.</given-names></name><name><surname>Kim</surname><given-names>J. M.</given-names></name><name><surname>Lee</surname><given-names>J.</given-names></name><name><surname>Yechoor</surname><given-names>V. K.</given-names></name><etal></etal></person-group>. (<year>2012</year>). <article-title>The clock gene, brain and muscle Arnt-like 1, regulates adipogenesis via Wnt signaling pathway</article-title>. <source>FASEB J</source>. <volume>26</volume>, <fpage>3453</fpage>–<lpage>3463</lpage>. <pub-id pub-id-type="doi">10.1096/fj.12-205781</pub-id><pub-id pub-id-type="pmid">22611086</pub-id></mixed-citation></ref><ref id="B61"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Haapaniemi</surname><given-names>T. H.</given-names></name><name><surname>Pursiainen</surname><given-names>V.</given-names></name><name><surname>Korpelainen</surname><given-names>J. T.</given-names></name><name><surname>Huikuri</surname><given-names>H. V.</given-names></name><name><surname>Sotaniemi</surname><given-names>K. A.</given-names></name><name><surname>Myllyla</surname><given-names>V. V.</given-names></name></person-group> (<year>2001</year>). <article-title>Ambulatory ECG and analysis of heart rate variability in Parkinson's disease</article-title>. <source>J. Neurol. Neurosurg. Psychiatry</source><volume>70</volume>, <fpage>305</fpage>–<lpage>310</lpage>. <pub-id pub-id-type="doi">10.1136/jnnp.70.3.305</pub-id><pub-id pub-id-type="pmid">11181850</pub-id></mixed-citation></ref><ref id="B62"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hack</surname><given-names>N.</given-names></name><name><surname>Fayad</surname><given-names>S. M.</given-names></name><name><surname>Monari</surname><given-names>E. H.</given-names></name><name><surname>Akbar</surname><given-names>U.</given-names></name><name><surname>Hardwick</surname><given-names>A.</given-names></name><name><surname>Rodriguez</surname><given-names>R. L.</given-names></name><etal></etal></person-group>. (<year>2014</year>). <article-title>An eight-year clinic experience with clozapine use in a Parkinson's disease clinic setting</article-title>. <source>PLoS ONE</source><volume>9</volume>:<fpage>e91545</fpage>. <pub-id pub-id-type="doi">10.1371/journal.pone.0091545</pub-id><pub-id pub-id-type="pmid">24646688</pub-id></mixed-citation></ref><ref id="B63"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Halabi</surname><given-names>C. M.</given-names></name><name><surname>Beyer</surname><given-names>A. M.</given-names></name><name><surname>de Lange</surname><given-names>W. J.</given-names></name><name><surname>Keen</surname><given-names>H. L.</given-names></name><name><surname>Baumbach</surname><given-names>G. L.</given-names></name><name><surname>Faraci</surname><given-names>F. M.</given-names></name><etal></etal></person-group>. (<year>2008</year>). <article-title>Interference with PPAR gamma function in smooth muscle causes vascular dysfunction and hypertension</article-title>. <source>Cell Metab</source>. <volume>7</volume>, <fpage>215</fpage>–<lpage>226</lpage>. <pub-id pub-id-type="doi">10.1016/j.cmet.2007.12.008</pub-id><pub-id pub-id-type="pmid">18316027</pub-id></mixed-citation></ref><ref id="B64"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hardin</surname><given-names>P. E.</given-names></name><name><surname>Hall</surname><given-names>J. C.</given-names></name><name><surname>Rosbash</surname><given-names>M.</given-names></name></person-group> (<year>1990</year>). <article-title>Feedback of the Drosophila period gene product on circadian cycling of its messenger RNA levels</article-title>. <source>Nature</source><volume>343</volume>, <fpage>536</fpage>–<lpage>540</lpage>. <pub-id pub-id-type="doi">10.1038/343536a0</pub-id><pub-id pub-id-type="pmid">2105471</pub-id></mixed-citation></ref><ref id="B65"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hebert</surname><given-names>J. L.</given-names></name><name><surname>Chemla</surname><given-names>D.</given-names></name><name><surname>Gerard</surname><given-names>O.</given-names></name><name><surname>Zamani</surname><given-names>K.</given-names></name><name><surname>Quillard</surname><given-names>J.</given-names></name><name><surname>Azarine</surname><given-names>A.</given-names></name><etal></etal></person-group>. (<year>2004</year>). <article-title>Angiographic right and left ventricular function in arrhythmogenic right ventricular dysplasia</article-title>. <source>Am. J. Cardiol</source>. <volume>93</volume>, <fpage>728</fpage>–<lpage>733</lpage>. <pub-id pub-id-type="doi">10.1016/j.amjcard.2003.11.055</pub-id><pub-id pub-id-type="pmid">15019878</pub-id></mixed-citation></ref><ref id="B66"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hedgepeth</surname><given-names>C. M.</given-names></name><name><surname>Conrad</surname><given-names>L. J.</given-names></name><name><surname>Zhang</surname><given-names>J.</given-names></name><name><surname>Huang</surname><given-names>H. C.</given-names></name><name><surname>Lee</surname><given-names>V. M.</given-names></name><name><surname>Klein</surname><given-names>P. S.</given-names></name></person-group> (<year>1997</year>). <article-title>Activation of the Wnt signaling pathway: a molecular mechanism for lithium action</article-title>. <source>Dev. Biol</source>. <volume>185</volume>, <fpage>82</fpage>–<lpage>91</lpage>. <pub-id pub-id-type="doi">10.1006/dbio.1997.8552</pub-id><pub-id pub-id-type="pmid">9169052</pub-id></mixed-citation></ref><ref id="B67"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hennekens</surname><given-names>C. H.</given-names></name><name><surname>Hennekens</surname><given-names>A. R.</given-names></name><name><surname>Hollar</surname><given-names>D.</given-names></name><name><surname>Casey</surname><given-names>D. E.</given-names></name></person-group> (<year>2005</year>). <article-title>Schizophrenia and increased risks of cardiovascular disease</article-title>. <source>Am. Heart J</source>. <volume>150</volume>, <fpage>1115</fpage>–<lpage>1121</lpage>. <pub-id pub-id-type="doi">10.1016/j.ahj.2005.02.007</pub-id><pub-id pub-id-type="pmid">16338246</pub-id></mixed-citation></ref><ref id="B68"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Heuberger</surname><given-names>J.</given-names></name><name><surname>Birchmeier</surname><given-names>W.</given-names></name></person-group> (<year>2010</year>). <article-title>Interplay of cadherin-mediated cell adhesion and canonical wnt signaling</article-title>. <source>Cold Spring Harb. Perspect. Biol</source>. <volume>2</volume>:<fpage>a002915</fpage>. <pub-id pub-id-type="doi">10.1101/cshperspect.a002915</pub-id><pub-id pub-id-type="pmid">20182623</pub-id></mixed-citation></ref><ref id="B69"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hineno</surname><given-names>T.</given-names></name><name><surname>Mizobuchi</surname><given-names>M.</given-names></name><name><surname>Hiratani</surname><given-names>K.</given-names></name><name><surname>Inami</surname><given-names>Y.</given-names></name><name><surname>Kakimoto</surname><given-names>Y.</given-names></name></person-group> (<year>1992</year>). <article-title>Disappearance of circadian rhythms in Parkinson's disease model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in dogs</article-title>. <source>Brain Res</source>. <volume>580</volume>, <fpage>92</fpage>–<lpage>99</lpage>. <pub-id pub-id-type="doi">10.1016/0006-8993(92)90930-8</pub-id><pub-id pub-id-type="pmid">1504821</pub-id></mixed-citation></ref><ref id="B70"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hogenesch</surname><given-names>J. B.</given-names></name><name><surname>Gu</surname><given-names>Y. Z.</given-names></name><name><surname>Jain</surname><given-names>S.</given-names></name><name><surname>Bradfield</surname><given-names>C. A.</given-names></name></person-group> (<year>1998</year>). <article-title>The basic-helix-loop-helix-PAS orphan MOP3 forms transcriptionally active complexes with circadian and hypoxia factors</article-title>. <source>Proc. Natl. Acad. Sci. U.S.A</source>. <volume>95</volume>, <fpage>5474</fpage>–<lpage>5479</lpage>. <pub-id pub-id-type="doi">10.1073/pnas.95.10.5474</pub-id><pub-id pub-id-type="pmid">9576906</pub-id></mixed-citation></ref><ref id="B71"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hu</surname><given-names>K.</given-names></name><name><surname>Ivanov</surname><given-names>P.</given-names></name><name><surname>Hilton</surname><given-names>M. F.</given-names></name><name><surname>Chen</surname><given-names>Z.</given-names></name><name><surname>Ayers</surname><given-names>R. T.</given-names></name><name><surname>Stanley</surname><given-names>H. E.</given-names></name><etal></etal></person-group>. (<year>2004</year>). <article-title>Endogenous circadian rhythm in an index of cardiac vulnerability independent of changes in behavior</article-title>. <source>Proc. Natl. Acad. Sci. U.S.A</source>. <volume>101</volume>, <fpage>18223</fpage>–<lpage>18227</lpage>. <pub-id pub-id-type="doi">10.1073/pnas.0408243101</pub-id><pub-id pub-id-type="pmid">15611476</pub-id></mixed-citation></ref><ref id="B72"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Huss</surname><given-names>J. M.</given-names></name><name><surname>Levy</surname><given-names>F. H.</given-names></name><name><surname>Kelly</surname><given-names>D. P.</given-names></name></person-group> (<year>2001</year>). <article-title>Hypoxia inhibits the peroxisome proliferator-activated receptor alpha/retinoid X receptor gene regulatory pathway in cardiac myocytes: a mechanism for O2-dependent modulation of mitochondrial fatty acid oxidation</article-title>. <source>J. Biol. Chem</source>. <volume>276</volume>, <fpage>27605</fpage>–<lpage>27612</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.M100277200</pub-id><pub-id pub-id-type="pmid">11371554</pub-id></mixed-citation></ref><ref id="B73"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Inestrosa</surname><given-names>N. C.</given-names></name><name><surname>Toledo</surname><given-names>E. M.</given-names></name></person-group> (<year>2008</year>). <article-title>The role of Wnt signaling in neuronal dysfunction in Alzheimer's Disease</article-title>. <source>Mol. Neurodegener</source>. <volume>3</volume>:<fpage>9</fpage>. <pub-id pub-id-type="doi">10.1186/1750-1326-3-9</pub-id><pub-id pub-id-type="pmid">18652670</pub-id></mixed-citation></ref><ref id="B74"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Inoue</surname><given-names>I.</given-names></name><name><surname>Shinoda</surname><given-names>Y.</given-names></name><name><surname>Ikeda</surname><given-names>M.</given-names></name><name><surname>Hayashi</surname><given-names>K.</given-names></name><name><surname>Kanazawa</surname><given-names>K.</given-names></name><name><surname>Nomura</surname><given-names>M.</given-names></name><etal></etal></person-group>. (<year>2005</year>). <article-title>CLOCK/BMAL1 is involved in lipid metabolism via transactivation of the peroxisome proliferator-activated receptor (PPAR) response element</article-title>. <source>J. Atheroscler. Thromb</source>. <volume>12</volume>, <fpage>169</fpage>–<lpage>174</lpage>. <pub-id pub-id-type="doi">10.5551/jat.12.169</pub-id><pub-id pub-id-type="pmid">16020918</pub-id></mixed-citation></ref><ref id="B75"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ip</surname><given-names>W.</given-names></name><name><surname>Chiang</surname><given-names>Y. T.</given-names></name><name><surname>Jin</surname><given-names>T.</given-names></name></person-group> (<year>2012</year>). <article-title>The involvement of the wnt signaling pathway and TCF7L2 in diabetes mellitus: the current understanding, dispute, and perspective</article-title>. <source>Cell Biosci</source>. <volume>2</volume>:<fpage>28</fpage>. <pub-id pub-id-type="doi">10.1186/2045-3701-2-28</pub-id><pub-id pub-id-type="pmid">22892353</pub-id></mixed-citation></ref><ref id="B76"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ivanov</surname><given-names>P.</given-names></name><name><surname>Hu</surname><given-names>K.</given-names></name><name><surname>Hilton</surname><given-names>M. F.</given-names></name><name><surname>Shea</surname><given-names>S. A.</given-names></name><name><surname>Stanley</surname><given-names>H. E.</given-names></name></person-group> (<year>2007</year>). <article-title>Endogenous circadian rhythm in human motor activity uncoupled from circadian influences on cardiac dynamics</article-title>. <source>Proc. Natl. Acad. Sci. U.S.A</source>. <volume>104</volume>, <fpage>20702</fpage>–<lpage>20707</lpage>. <pub-id pub-id-type="doi">10.1073/pnas.0709957104</pub-id><pub-id pub-id-type="pmid">18093917</pub-id></mixed-citation></ref><ref id="B77"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jadidi</surname><given-names>E.</given-names></name><name><surname>Mohammadi</surname><given-names>M.</given-names></name><name><surname>Moradi</surname><given-names>T.</given-names></name></person-group> (<year>2013</year>). <article-title>High risk of cardiovascular diseases after diagnosis of multiple sclerosis</article-title>. <source>Mult. Scler</source>. <volume>19</volume>, <fpage>1336</fpage>–<lpage>1340</lpage>. <pub-id pub-id-type="doi">10.1177/1352458513475833</pub-id><pub-id pub-id-type="pmid">23364857</pub-id></mixed-citation></ref><ref id="B78"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jansson</surname><given-names>E. A.</given-names></name><name><surname>Are</surname><given-names>A.</given-names></name><name><surname>Greicius</surname><given-names>G.</given-names></name><name><surname>Kuo</surname><given-names>I. C.</given-names></name><name><surname>Kelly</surname><given-names>D.</given-names></name><name><surname>Arulampalam</surname><given-names>V.</given-names></name><etal></etal></person-group>. (<year>2005</year>). <article-title>The Wnt/beta-catenin signaling pathway targets PPARgamma activity in colon cancer cells</article-title>. <source>Proc. Natl. Acad. Sci. U.S.A</source>. <volume>102</volume>, <fpage>1460</fpage>–<lpage>1465</lpage>. <pub-id pub-id-type="doi">10.1073/pnas.0405928102</pub-id><pub-id pub-id-type="pmid">15665104</pub-id></mixed-citation></ref><ref id="B79"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jiang</surname><given-names>Q.</given-names></name><name><surname>Heneka</surname><given-names>M.</given-names></name><name><surname>Landreth</surname><given-names>G. E.</given-names></name></person-group> (<year>2008</year>). <article-title>The role of peroxisome proliferator-activated receptor-gamma (PPARgamma) in Alzheimer's disease: therapeutic implications</article-title>. <source>CNS Drugs</source><volume>22</volume>, <fpage>1</fpage>–<lpage>14</lpage>. <pub-id pub-id-type="doi">10.2165/00023210-200822010-00001</pub-id><pub-id pub-id-type="pmid">18072811</pub-id></mixed-citation></ref><ref id="B80"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kawai</surname><given-names>M.</given-names></name><name><surname>Green</surname><given-names>C. B.</given-names></name><name><surname>Lecka-Czernik</surname><given-names>B.</given-names></name><name><surname>Douris</surname><given-names>N.</given-names></name><name><surname>Gilbert</surname><given-names>M. R.</given-names></name><name><surname>Kojima</surname><given-names>S.</given-names></name><etal></etal></person-group>. (<year>2010</year>). <article-title>A circadian-regulated gene, Nocturnin, promotes adipogenesis by stimulating PPAR-gamma nuclear translocation</article-title>. <source>Proc. Natl. Acad. Sci. U.S.A</source>. <volume>107</volume>, <fpage>10508</fpage>–<lpage>10513</lpage>. <pub-id pub-id-type="doi">10.1073/pnas.1000788107</pub-id><pub-id pub-id-type="pmid">20498072</pub-id></mixed-citation></ref><ref id="B81"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kelly</surname><given-names>D. P.</given-names></name></person-group> (<year>2003</year>). <article-title>PPARs of the heart: three is a crowd</article-title>. <source>Circ. Res</source>. <volume>92</volume>, <fpage>482</fpage>–<lpage>484</lpage>. <pub-id pub-id-type="doi">10.1161/01.RES.0000064382.46274.95</pub-id><pub-id pub-id-type="pmid">12649261</pub-id></mixed-citation></ref><ref id="B82"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kiaei</surname><given-names>M.</given-names></name></person-group> (<year>2008</year>). <article-title>Peroxisome proliferator-activated receptor-gamma in amyotrophic lateral sclerosis and Huntington's disease</article-title>. <source>PPAR Res</source>. <volume>2008</volume>:<fpage>418765</fpage>. <pub-id pub-id-type="doi">10.1155/2008/418765</pub-id><pub-id pub-id-type="pmid">18464922</pub-id></mixed-citation></ref><ref id="B83"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kiriazis</surname><given-names>H.</given-names></name><name><surname>Jennings</surname><given-names>N. L.</given-names></name><name><surname>Davern</surname><given-names>P.</given-names></name><name><surname>Lambert</surname><given-names>G.</given-names></name><name><surname>Su</surname><given-names>Y.</given-names></name><name><surname>Pang</surname><given-names>T.</given-names></name><etal></etal></person-group>. (<year>2012</year>). <article-title>Neurocardiac dysregulation and neurogenic arrhythmias in a transgenic mouse model of Huntington's disease</article-title>. <source>J. Physiol</source>. <volume>590</volume>, <fpage>5845</fpage>–<lpage>5860</lpage>. <pub-id pub-id-type="doi">10.1113/jphysiol.2012.238113</pub-id><pub-id pub-id-type="pmid">22890713</pub-id></mixed-citation></ref><ref id="B84"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Klymkowsky</surname><given-names>M. W.</given-names></name><name><surname>Williams</surname><given-names>B. O.</given-names></name><name><surname>Barish</surname><given-names>G. D.</given-names></name><name><surname>Varmus</surname><given-names>H. E.</given-names></name><name><surname>Vourgourakis</surname><given-names>Y. E.</given-names></name></person-group> (<year>1999</year>). <article-title>Membrane-anchored plakoglobins have multiple mechanisms of action in Wnt signaling</article-title>. <source>Mol. Biol. Cell</source><volume>10</volume>, <fpage>3151</fpage>–<lpage>3169</lpage>. <pub-id pub-id-type="doi">10.1091/mbc.10.10.3151</pub-id><pub-id pub-id-type="pmid">10512857</pub-id></mixed-citation></ref><ref id="B85"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kolker</surname><given-names>D. E.</given-names></name><name><surname>Fukuyama</surname><given-names>H.</given-names></name><name><surname>Huang</surname><given-names>D. S.</given-names></name><name><surname>Takahashi</surname><given-names>J. S.</given-names></name><name><surname>Horton</surname><given-names>T. H.</given-names></name><name><surname>Turek</surname><given-names>F. W.</given-names></name></person-group> (<year>2003</year>). <article-title>Aging alters circadian and light-induced expression of clock genes in golden hamsters</article-title>. <source>J. Biol. Rhythms</source><volume>18</volume>, <fpage>159</fpage>–<lpage>169</lpage>. <pub-id pub-id-type="doi">10.1177/0748730403251802</pub-id><pub-id pub-id-type="pmid">12693870</pub-id></mixed-citation></ref><ref id="B86"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Korvala</surname><given-names>J.</given-names></name><name><surname>Juppner</surname><given-names>H.</given-names></name><name><surname>Makitie</surname><given-names>O.</given-names></name><name><surname>Sochett</surname><given-names>E.</given-names></name><name><surname>Schnabel</surname><given-names>D.</given-names></name><name><surname>Mora</surname><given-names>S.</given-names></name><etal></etal></person-group>. (<year>2012</year>). <article-title>Mutations in LRP5 cause primary osteoporosis without features of OI by reducing Wnt signaling activity</article-title>. <source>BMC Med. Genet</source>. <volume>13</volume>:<fpage>26</fpage>. <pub-id pub-id-type="doi">10.1186/1471-2350-13-26</pub-id><pub-id pub-id-type="pmid">22487062</pub-id></mixed-citation></ref><ref id="B87"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kremer</surname><given-names>H. P.</given-names></name><name><surname>Roos</surname><given-names>R. A.</given-names></name><name><surname>Dingjan</surname><given-names>G. M.</given-names></name><name><surname>Bots</surname><given-names>G. T.</given-names></name><name><surname>Bruyn</surname><given-names>G. W.</given-names></name><name><surname>Hofman</surname><given-names>M. A.</given-names></name></person-group> (<year>1991</year>). <article-title>The hypothalamic lateral tuberal nucleus and the characteristics of neuronal loss in Huntington's disease</article-title>. <source>Neurosci. Lett</source>. <volume>132</volume>, <fpage>101</fpage>–<lpage>104</lpage>. <pub-id pub-id-type="doi">10.1016/0304-3940(91)90443-W</pub-id><pub-id pub-id-type="pmid">1838577</pub-id></mixed-citation></ref><ref id="B88"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Krishnan</surname><given-names>J.</given-names></name><name><surname>Suter</surname><given-names>M.</given-names></name><name><surname>Windak</surname><given-names>R.</given-names></name><name><surname>Krebs</surname><given-names>T.</given-names></name><name><surname>Felley</surname><given-names>A.</given-names></name><name><surname>Montessuit</surname><given-names>C.</given-names></name><etal></etal></person-group>. (<year>2009</year>). <article-title>Activation of a HIF1alpha-PPARgamma axis underlies the integration of glycolytic and lipid anabolic pathways in pathologic cardiac hypertrophy</article-title>. <source>Cell Metab</source>. <volume>9</volume>, <fpage>512</fpage>–<lpage>524</lpage>. <pub-id pub-id-type="doi">10.1016/j.cmet.2009.05.005</pub-id><pub-id pub-id-type="pmid">19490906</pub-id></mixed-citation></ref><ref id="B89"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kume</surname><given-names>K.</given-names></name><name><surname>Zylka</surname><given-names>M. J.</given-names></name><name><surname>Sriram</surname><given-names>S.</given-names></name><name><surname>Shearman</surname><given-names>L. P.</given-names></name><name><surname>Weaver</surname><given-names>D. R.</given-names></name><name><surname>Jin</surname><given-names>X.</given-names></name><etal></etal></person-group>. (<year>1999</year>). <article-title>mCRY1 and mCRY2 are essential components of the negative limb of the circadian clock feedback loop</article-title>. <source>Cell</source><volume>98</volume>, <fpage>193</fpage>–<lpage>205</lpage>. <pub-id pub-id-type="doi">10.1016/S0092-8674(00)81014-4</pub-id><pub-id pub-id-type="pmid">10428031</pub-id></mixed-citation></ref><ref id="B90"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lan</surname><given-names>M. J.</given-names></name><name><surname>Yuan</surname><given-names>P.</given-names></name><name><surname>Chen</surname><given-names>G.</given-names></name><name><surname>Manji</surname><given-names>H. K.</given-names></name></person-group> (<year>2008</year>). <article-title>Neuronal peroxisome proliferator-activated receptor gamma signaling: regulation by mood-stabilizer valproate</article-title>. <source>J. Mol. Neurosci</source>. <volume>35</volume>, <fpage>225</fpage>–<lpage>234</lpage>. <pub-id pub-id-type="doi">10.1007/s12031-008-9056-8</pub-id><pub-id pub-id-type="pmid">18437585</pub-id></mixed-citation></ref><ref id="B91"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lecarpentier</surname><given-names>Y.</given-names></name><name><surname>Claes</surname><given-names>V.</given-names></name><name><surname>Hebert</surname><given-names>J. L.</given-names></name></person-group> (<year>2010</year>). <article-title>PPARs, cardiovascular metabolism, and function: near- or far-from-equilibrium pathways</article-title>. <source>PPAR Res</source>. <volume>2010</volume>:<fpage>783273</fpage>. <pub-id pub-id-type="doi">10.1155/2010/783273</pub-id><pub-id pub-id-type="pmid">20706650</pub-id></mixed-citation></ref><ref id="B92"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lee</surname><given-names>D. K.</given-names></name><name><surname>Nathan Grantham</surname><given-names>R.</given-names></name><name><surname>Trachte</surname><given-names>A. L.</given-names></name><name><surname>Mannion</surname><given-names>J. D.</given-names></name><name><surname>Wilson</surname><given-names>C. L.</given-names></name></person-group> (<year>2006</year>). <article-title>Activation of the canonical Wnt/beta-catenin pathway enhances monocyte adhesion to endothelial cells</article-title>. <source>Biochem. Biophys. Res. Commun</source>. <volume>347</volume>, <fpage>109</fpage>–<lpage>116</lpage>. <pub-id pub-id-type="doi">10.1016/j.bbrc.2006.06.082</pub-id><pub-id pub-id-type="pmid">16815294</pub-id></mixed-citation></ref><ref id="B93"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Leibetseder</surname><given-names>V.</given-names></name><name><surname>Humpeler</surname><given-names>S.</given-names></name><name><surname>Svoboda</surname><given-names>M.</given-names></name><name><surname>Schmid</surname><given-names>D.</given-names></name><name><surname>Thalhammer</surname><given-names>T.</given-names></name><name><surname>Zuckermann</surname><given-names>A.</given-names></name><etal></etal></person-group>. (<year>2009</year>). <article-title>Clock genes display rhythmic expression in human hearts</article-title>. <source>Chronobiol. Int</source>. <volume>26</volume>, <fpage>621</fpage>–<lpage>636</lpage>. <pub-id pub-id-type="doi">10.1080/07420520902924939</pub-id><pub-id pub-id-type="pmid">19444745</pub-id></mixed-citation></ref><ref id="B94"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lemberger</surname><given-names>T.</given-names></name><name><surname>Saladin</surname><given-names>R.</given-names></name><name><surname>Vazquez</surname><given-names>M.</given-names></name><name><surname>Assimacopoulos</surname><given-names>F.</given-names></name><name><surname>Staels</surname><given-names>B.</given-names></name><name><surname>Desvergne</surname><given-names>B.</given-names></name><etal></etal></person-group>. (<year>1996</year>). <article-title>Expression of the peroxisome proliferator-activated receptor alpha gene is stimulated by stress and follows a diurnal rhythm</article-title>. <source>J. Biol. Chem</source>. <volume>271</volume>, <fpage>1764</fpage>–<lpage>1769</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.271.3.1764</pub-id><pub-id pub-id-type="pmid">8576180</pub-id></mixed-citation></ref><ref id="B95"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lemberger</surname><given-names>T.</given-names></name><name><surname>Staels</surname><given-names>B.</given-names></name><name><surname>Saladin</surname><given-names>R.</given-names></name><name><surname>Desvergne</surname><given-names>B.</given-names></name><name><surname>Auwerx</surname><given-names>J.</given-names></name><name><surname>Wahli</surname><given-names>W.</given-names></name></person-group> (<year>1994</year>). <article-title>Regulation of the peroxisome proliferator-activated receptor alpha gene by glucocorticoids</article-title>. <source>J. Biol. Chem</source>. <volume>269</volume>, <fpage>24527</fpage>–<lpage>24530</lpage>. <pub-id pub-id-type="pmid">7929119</pub-id></mixed-citation></ref><ref id="B96"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>L'Episcopo</surname><given-names>F.</given-names></name><name><surname>Serapide</surname><given-names>M. F.</given-names></name><name><surname>Tirolo</surname><given-names>C.</given-names></name><name><surname>Testa</surname><given-names>N.</given-names></name><name><surname>Caniglia</surname><given-names>S.</given-names></name><name><surname>Morale</surname><given-names>M. C.</given-names></name><etal></etal></person-group>. (<year>2011</year>). <article-title>A Wnt1 regulated Frizzled-1/beta-Catenin signaling pathway as a candidate regulatory circuit controlling mesencephalic dopaminergic neuron-astrocyte crosstalk: therapeutical relevance for neuron survival and neuroprotection</article-title>. <source>Mol. Neurodegener</source>. <volume>6</volume>:<fpage>49</fpage>. <pub-id pub-id-type="doi">10.1186/1750-1326-6-49</pub-id><pub-id pub-id-type="pmid">21752258</pub-id></mixed-citation></ref><ref id="B97"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>L'Episcopo</surname><given-names>F.</given-names></name><name><surname>Tirolo</surname><given-names>C.</given-names></name><name><surname>Testa</surname><given-names>N.</given-names></name><name><surname>Caniglia</surname><given-names>S.</given-names></name><name><surname>Morale</surname><given-names>M. C.</given-names></name><name><surname>Deleidi</surname><given-names>M.</given-names></name><etal></etal></person-group>. (<year>2012</year>). <article-title>Plasticity of subventricular zone neuroprogenitors in MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson's disease involves cross talk between inflammatory and Wnt/beta-catenin signaling pathways: functional consequences for neuroprotection and repair</article-title>. <source>J. Neurosci</source>. <volume>32</volume>, <fpage>2062</fpage>–<lpage>2085</lpage>. <pub-id pub-id-type="doi">10.1523/JNEUROSCI.5259-11.2012</pub-id><pub-id pub-id-type="pmid">22323720</pub-id></mixed-citation></ref><ref id="B98"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liang</surname><given-names>H.</given-names></name><name><surname>Ward</surname><given-names>W. F.</given-names></name></person-group> (<year>2006</year>). <article-title>PGC-1alpha: a key regulator of energy metabolism</article-title>. <source>Adv. Physiol. Educ</source>. <volume>30</volume>, <fpage>145</fpage>–<lpage>151</lpage>. <pub-id pub-id-type="doi">10.1152/advan.00052.2006</pub-id><pub-id pub-id-type="pmid">17108241</pub-id></mixed-citation></ref><ref id="B99"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>C.</given-names></name><name><surname>Li</surname><given-names>S.</given-names></name><name><surname>Liu</surname><given-names>T.</given-names></name><name><surname>Borjigin</surname><given-names>J.</given-names></name><name><surname>Lin</surname><given-names>J. D.</given-names></name></person-group> (<year>2007a</year>). <article-title>Transcriptional coactivator PGC-1alpha integrates the mammalian clock and energy metabolism</article-title>. <source>Nature</source><volume>447</volume>, <fpage>477</fpage>–<lpage>481</lpage>. <pub-id pub-id-type="doi">10.1038/nature05767</pub-id><pub-id pub-id-type="pmid">17476214</pub-id></mixed-citation></ref><ref id="B100"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>H.</given-names></name><name><surname>Fergusson</surname><given-names>M. M.</given-names></name><name><surname>Castilho</surname><given-names>R. M.</given-names></name><name><surname>Liu</surname><given-names>J.</given-names></name><name><surname>Cao</surname><given-names>L.</given-names></name><name><surname>Chen</surname><given-names>J.</given-names></name><etal></etal></person-group>. (<year>2007b</year>). <article-title>Augmented Wnt signaling in a mammalian model of accelerated aging</article-title>. <source>Science</source><volume>317</volume>, <fpage>803</fpage>–<lpage>806</lpage>. <pub-id pub-id-type="doi">10.1126/science.1143578</pub-id><pub-id pub-id-type="pmid">17690294</pub-id></mixed-citation></ref><ref id="B101"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lockyer</surname><given-names>P.</given-names></name><name><surname>Schisler</surname><given-names>J. C.</given-names></name><name><surname>Patterson</surname><given-names>C.</given-names></name><name><surname>Willis</surname><given-names>M. S.</given-names></name></person-group> (<year>2009</year>). <article-title>Minireview: won't get fooled again: the nonmetabolic roles of peroxisome proliferator-activated receptors (PPARs) in the heart</article-title>. <source>Mol. Endocrinol</source>. <volume>24</volume>, <fpage>1111</fpage>–<lpage>1119</lpage>. <pub-id pub-id-type="doi">10.1210/me.2009-0374</pub-id><pub-id pub-id-type="pmid">20016041</pub-id></mixed-citation></ref><ref id="B102"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lo Coco</surname><given-names>D.</given-names></name><name><surname>Mattaliano</surname><given-names>P.</given-names></name><name><surname>Spataro</surname><given-names>R.</given-names></name><name><surname>Mattaliano</surname><given-names>A.</given-names></name><name><surname>La Bella</surname><given-names>V.</given-names></name></person-group> (<year>2011</year>). <article-title>Sleep-wake disturbances in patients with amyotrophic lateral sclerosis</article-title>. <source>J. Neurol. Neurosurg. Psychiatry</source><volume>82</volume>, <fpage>839</fpage>–<lpage>842</lpage>. <pub-id pub-id-type="doi">10.1136/jnnp.2010.228007</pub-id><pub-id pub-id-type="pmid">21217159</pub-id></mixed-citation></ref><ref id="B103"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lu</surname><given-names>D.</given-names></name><name><surname>Carson</surname><given-names>D. A.</given-names></name></person-group> (<year>2010</year>). <article-title>Repression of beta-catenin signaling by PPAR gamma ligands</article-title>. <source>Eur. J. Pharmacol</source>. <volume>636</volume>, <fpage>198</fpage>–<lpage>202</lpage>. <pub-id pub-id-type="doi">10.1016/j.ejphar.2010.03.010</pub-id><pub-id pub-id-type="pmid">20303941</pub-id></mixed-citation></ref><ref id="B104"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>MacDonald</surname><given-names>B. T.</given-names></name><name><surname>Tamai</surname><given-names>K.</given-names></name><name><surname>He</surname><given-names>X.</given-names></name></person-group> (<year>2009</year>). <article-title>Wnt/beta-catenin signaling: components, mechanisms, and diseases</article-title>. <source>Dev. Cell</source><volume>17</volume>, <fpage>9</fpage>–<lpage>26</lpage>. <pub-id pub-id-type="doi">10.1016/j.devcel.2009.06.016</pub-id><pub-id pub-id-type="pmid">19619488</pub-id></mixed-citation></ref><ref id="B105"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Maeda</surname><given-names>O.</given-names></name><name><surname>Usami</surname><given-names>N.</given-names></name><name><surname>Kondo</surname><given-names>M.</given-names></name><name><surname>Takahashi</surname><given-names>M.</given-names></name><name><surname>Goto</surname><given-names>H.</given-names></name><name><surname>Shimokata</surname><given-names>K.</given-names></name><etal></etal></person-group>. (<year>2004</year>). <article-title>Plakoglobin (gamma-catenin) has TCF/LEF family-dependent transcriptional activity in beta-catenin-deficient cell line</article-title>. <source>Oncogene</source><volume>23</volume>, <fpage>964</fpage>–<lpage>972</lpage>. <pub-id pub-id-type="doi">10.1038/sj.onc.1207254</pub-id><pub-id pub-id-type="pmid">14661054</pub-id></mixed-citation></ref><ref id="B106"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Marcheva</surname><given-names>B.</given-names></name><name><surname>Ramsey</surname><given-names>K. M.</given-names></name><name><surname>Buhr</surname><given-names>E. D.</given-names></name><name><surname>Kobayashi</surname><given-names>Y.</given-names></name><name><surname>Su</surname><given-names>H.</given-names></name><name><surname>Ko</surname><given-names>C. H.</given-names></name><etal></etal></person-group>. (<year>2010</year>). <article-title>Disruption of the clock components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes</article-title>. <source>Nature</source><volume>466</volume>, <fpage>627</fpage>–<lpage>631</lpage>. <pub-id pub-id-type="doi">10.1038/nature09253</pub-id><pub-id pub-id-type="pmid">20562852</pub-id></mixed-citation></ref><ref id="B107"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Marcus</surname><given-names>F. I.</given-names></name><name><surname>Fontaine</surname><given-names>G. H.</given-names></name><name><surname>Guiraudon</surname><given-names>G.</given-names></name><name><surname>Frank</surname><given-names>R.</given-names></name><name><surname>Laurenceau</surname><given-names>J. L.</given-names></name><name><surname>Malergue</surname><given-names>C.</given-names></name><etal></etal></person-group>. (<year>1982</year>). <article-title>Right ventricular dysplasia: a report of 24 adult cases</article-title>. <source>Circulation</source><volume>65</volume>, <fpage>384</fpage>–<lpage>398</lpage>. <pub-id pub-id-type="doi">10.1161/01.CIR.65.2.384</pub-id><pub-id pub-id-type="pmid">7053899</pub-id></mixed-citation></ref><ref id="B108"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Marmolino</surname><given-names>D.</given-names></name><name><surname>Acquaviva</surname><given-names>F.</given-names></name><name><surname>Pinelli</surname><given-names>M.</given-names></name><name><surname>Monticelli</surname><given-names>A.</given-names></name><name><surname>Castaldo</surname><given-names>I.</given-names></name><name><surname>Filla</surname><given-names>A.</given-names></name><etal></etal></person-group>. (<year>2009</year>). <article-title>PPAR-gamma agonist Azelaoyl PAF increases frataxin protein and mRNA expression: new implications for the Friedreich's ataxia therapy</article-title>. <source>Cerebellum</source><volume>8</volume>, <fpage>98</fpage>–<lpage>103</lpage>. <pub-id pub-id-type="doi">10.1007/s12311-008-0087-z</pub-id><pub-id pub-id-type="pmid">19104905</pub-id></mixed-citation></ref><ref id="B109"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Maywood</surname><given-names>E. S.</given-names></name><name><surname>Fraenkel</surname><given-names>E.</given-names></name><name><surname>McAllister</surname><given-names>C. J.</given-names></name><name><surname>Wood</surname><given-names>N.</given-names></name><name><surname>Reddy</surname><given-names>A. B.</given-names></name><name><surname>Hastings</surname><given-names>M. H.</given-names></name><etal></etal></person-group>. (<year>2010</year>). <article-title>Disruption of peripheral circadian timekeeping in a mouse model of Huntington's disease and its restoration by temporally scheduled feeding</article-title>. <source>J. Neurosci</source>. <volume>30</volume>, <fpage>10199</fpage>–<lpage>10204</lpage>. <pub-id pub-id-type="doi">10.1523/JNEUROSCI.1694-10.2010</pub-id><pub-id pub-id-type="pmid">20668203</pub-id></mixed-citation></ref><ref id="B110"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>McNamara</surname><given-names>P.</given-names></name><name><surname>Seo</surname><given-names>S. B.</given-names></name><name><surname>Rudic</surname><given-names>R. D.</given-names></name><name><surname>Sehgal</surname><given-names>A.</given-names></name><name><surname>Chakravarti</surname><given-names>D.</given-names></name><name><surname>FitzGerald</surname><given-names>G. A.</given-names></name></person-group> (<year>2001</year>). <article-title>Regulation of CLOCK and MOP4 by nuclear hormone receptors in the vasculature: a humoral mechanism to reset a peripheral clock</article-title>. <source>Cell</source><volume>105</volume>, <fpage>877</fpage>–<lpage>889</lpage>. <pub-id pub-id-type="doi">10.1016/S0092-8674(01)00401-9</pub-id><pub-id pub-id-type="pmid">11439184</pub-id></mixed-citation></ref><ref id="B111"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Meshorer</surname><given-names>E.</given-names></name><name><surname>Gruenbaum</surname><given-names>Y.</given-names></name></person-group> (<year>2008</year>). <article-title>Gone with the Wnt/Notch: stem cells in laminopathies, progeria, and aging</article-title>. <source>J. Cell Biol</source>. <volume>181</volume>, <fpage>9</fpage>–<lpage>13</lpage>. <pub-id pub-id-type="doi">10.1083/jcb.200802155</pub-id><pub-id pub-id-type="pmid">18378774</pub-id></mixed-citation></ref><ref id="B112"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mihm</surname><given-names>M. J.</given-names></name><name><surname>Amann</surname><given-names>D. M.</given-names></name><name><surname>Schanbacher</surname><given-names>B. L.</given-names></name><name><surname>Altschuld</surname><given-names>R. A.</given-names></name><name><surname>Bauer</surname><given-names>J. A.</given-names></name><name><surname>Hoyt</surname><given-names>K. R.</given-names></name></person-group> (<year>2007</year>). <article-title>Cardiac dysfunction in the R6/2 mouse model of Huntington's disease</article-title>. <source>Neurobiol. Dis</source>. <volume>25</volume>, <fpage>297</fpage>–<lpage>308</lpage>. <pub-id pub-id-type="doi">10.1016/j.nbd.2006.09.016</pub-id><pub-id pub-id-type="pmid">17126554</pub-id></mixed-citation></ref><ref id="B113"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Moldes</surname><given-names>M.</given-names></name><name><surname>Zuo</surname><given-names>Y.</given-names></name><name><surname>Morrison</surname><given-names>R. F.</given-names></name><name><surname>Silva</surname><given-names>D.</given-names></name><name><surname>Park</surname><given-names>B. H.</given-names></name><name><surname>Liu</surname><given-names>J.</given-names></name><etal></etal></person-group>. (<year>2003</year>). <article-title>Peroxisome-proliferator-activated receptor gamma suppresses Wnt/beta-catenin signalling during adipogenesis</article-title>. <source>Biochem. J</source>. <volume>376</volume>, <fpage>607</fpage>–<lpage>613</lpage>. <pub-id pub-id-type="doi">10.1042/BJ20030426</pub-id><pub-id pub-id-type="pmid">12954078</pub-id></mixed-citation></ref><ref id="B114"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Moon</surname><given-names>R. T.</given-names></name><name><surname>Bowerman</surname><given-names>B.</given-names></name><name><surname>Boutros</surname><given-names>M.</given-names></name><name><surname>Perrimon</surname><given-names>N.</given-names></name></person-group> (<year>2002</year>). <article-title>The promise and perils of Wnt signaling through beta-catenin</article-title>. <source>Science</source><volume>296</volume>, <fpage>1644</fpage>–<lpage>1646</lpage>. <pub-id pub-id-type="doi">10.1126/science.1071549</pub-id><pub-id pub-id-type="pmid">12040179</pub-id></mixed-citation></ref><ref id="B115"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Morin</surname><given-names>P. J.</given-names></name><name><surname>Sparks</surname><given-names>A. B.</given-names></name><name><surname>Korinek</surname><given-names>V.</given-names></name><name><surname>Barker</surname><given-names>N.</given-names></name><name><surname>Clevers</surname><given-names>H.</given-names></name><name><surname>Vogelstein</surname><given-names>B.</given-names></name><etal></etal></person-group>. (<year>1997</year>). <article-title>Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC</article-title>. <source>Science</source><volume>275</volume>, <fpage>1787</fpage>–<lpage>1790</lpage>. <pub-id pub-id-type="doi">10.1126/science.275.5307.1787</pub-id><pub-id pub-id-type="pmid">9065402</pub-id></mixed-citation></ref><ref id="B116"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Musiek</surname><given-names>E. S.</given-names></name><name><surname>Lim</surname><given-names>M. M.</given-names></name><name><surname>Yang</surname><given-names>G.</given-names></name><name><surname>Bauer</surname><given-names>A. Q.</given-names></name><name><surname>Qi</surname><given-names>L.</given-names></name><name><surname>Lee</surname><given-names>Y.</given-names></name><etal></etal></person-group>. (<year>2013</year>). <article-title>Circadian clock proteins regulate neuronal redox homeostasis and neurodegeneration</article-title>. <source>J. Clin. Invest</source>. <volume>123</volume>, <fpage>5389</fpage>–<lpage>5400</lpage>. <pub-id pub-id-type="doi">10.1172/JCI70317</pub-id><pub-id pub-id-type="pmid">24270424</pub-id></mixed-citation></ref><ref id="B117"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Naito</surname><given-names>A. T.</given-names></name><name><surname>Shiojima</surname><given-names>I.</given-names></name><name><surname>Komuro</surname><given-names>I.</given-names></name></person-group> (<year>2010</year>). <article-title>Wnt signaling and aging-related heart disorders</article-title>. <source>Circ. Res</source>. <volume>107</volume>, <fpage>1295</fpage>–<lpage>1303</lpage>. <pub-id pub-id-type="doi">10.1161/CIRCRESAHA.110.223776</pub-id><pub-id pub-id-type="pmid">21106946</pub-id></mixed-citation></ref><ref id="B118"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Najdi</surname><given-names>R.</given-names></name><name><surname>Holcombe</surname><given-names>R. F.</given-names></name><name><surname>Waterman</surname><given-names>M. L.</given-names></name></person-group> (<year>2011</year>). <article-title>Wnt signaling and colon carcinogenesis: beyond APC</article-title>. <source>J. Carcinog</source>. <volume>10</volume>:<fpage>5</fpage>. <pub-id pub-id-type="doi">10.4103/1477-3163.78111</pub-id><pub-id pub-id-type="pmid">21483657</pub-id></mixed-citation></ref><ref id="B119"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Narravula</surname><given-names>S.</given-names></name><name><surname>Colgan</surname><given-names>S. P.</given-names></name></person-group> (<year>2001</year>). <article-title>Hypoxia-inducible factor 1-mediated inhibition of peroxisome proliferator-activated receptor alpha expression during hypoxia</article-title>. <source>J. Immunol</source>. <volume>166</volume>, <fpage>7543</fpage>–<lpage>7548</lpage>. <pub-id pub-id-type="doi">10.4049/jimmunol.166.12.7543</pub-id><pub-id pub-id-type="pmid">11390509</pub-id></mixed-citation></ref><ref id="B120"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Nicol</surname><given-names>C. J.</given-names></name><name><surname>Adachi</surname><given-names>M.</given-names></name><name><surname>Akiyama</surname><given-names>T. E.</given-names></name><name><surname>Gonzalez</surname><given-names>F. J.</given-names></name></person-group> (<year>2005</year>). <article-title>PPARgamma in endothelial cells influences high fat diet-induced hypertension</article-title>. <source>Am. J. Hypertens</source>. <volume>18</volume>, <fpage>549</fpage>–<lpage>556</lpage>. <pub-id pub-id-type="doi">10.1016/j.amjhyper.2004.10.032</pub-id><pub-id pub-id-type="pmid">15831367</pub-id></mixed-citation></ref><ref id="B121"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Nonaka</surname><given-names>H.</given-names></name><name><surname>Emoto</surname><given-names>N.</given-names></name><name><surname>Ikeda</surname><given-names>K.</given-names></name><name><surname>Fukuya</surname><given-names>H.</given-names></name><name><surname>Rohman</surname><given-names>M. S.</given-names></name><name><surname>Raharjo</surname><given-names>S. B.</given-names></name><etal></etal></person-group>. (<year>2001</year>). <article-title>Angiotensin II induces circadian gene expression of clock genes in cultured vascular smooth muscle cells</article-title>. <source>Circulation</source><volume>104</volume>, <fpage>1746</fpage>–<lpage>1748</lpage>. <pub-id pub-id-type="doi">10.1161/hc4001.098048</pub-id><pub-id pub-id-type="pmid">11591607</pub-id></mixed-citation></ref><ref id="B122"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Oishi</surname><given-names>K.</given-names></name><name><surname>Shirai</surname><given-names>H.</given-names></name><name><surname>Ishida</surname><given-names>N.</given-names></name></person-group> (<year>2005</year>). <article-title>CLOCK is involved in the circadian transactivation of peroxisome-proliferator-activated receptor alpha (PPARalpha) in mice</article-title>. <source>Biochem. J</source>. <volume>386</volume>, <fpage>575</fpage>–<lpage>581</lpage>. <pub-id pub-id-type="doi">10.1042/BJ20041150</pub-id><pub-id pub-id-type="pmid">15500444</pub-id></mixed-citation></ref><ref id="B123"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Oishi</surname><given-names>K.</given-names></name><name><surname>Shirai</surname><given-names>H.</given-names></name><name><surname>Ishida</surname><given-names>N.</given-names></name></person-group> (<year>2008</year>). <article-title>PPARalpha is involved in photoentrainment of the circadian clock</article-title>. <source>Neuroreport</source><volume>19</volume>, <fpage>487</fpage>–<lpage>489</lpage>. <pub-id pub-id-type="doi">10.1097/WNR.0b013e3282f7968f</pub-id><pub-id pub-id-type="pmid">18287953</pub-id></mixed-citation></ref><ref id="B124"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>O'Neal</surname><given-names>W. T.</given-names></name><name><surname>Griffin</surname><given-names>W. F.</given-names></name><name><surname>Dries-Devlin</surname><given-names>J. L.</given-names></name><name><surname>Kent</surname><given-names>S. D.</given-names></name><name><surname>Chen</surname><given-names>J.</given-names></name><name><surname>Willis</surname><given-names>M. S.</given-names></name><etal></etal></person-group>. (<year>2013</year>). <article-title>Ephrin-Eph signaling as a potential therapeutic target for the treatment of myocardial infarction</article-title>. <source>Med. Hypotheses</source><volume>80</volume>, <fpage>738</fpage>–<lpage>744</lpage>. <pub-id pub-id-type="doi">10.1016/j.mehy.2013.02.024</pub-id><pub-id pub-id-type="pmid">23562676</pub-id></mixed-citation></ref><ref id="B125"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pallier</surname><given-names>P. N.</given-names></name><name><surname>Morton</surname><given-names>A. J.</given-names></name></person-group> (<year>2009</year>). <article-title>Management of sleep/wake cycles improves cognitive function in a transgenic mouse model of Huntington's disease</article-title>. <source>Brain Res</source>. <volume>1279</volume>, <fpage>90</fpage>–<lpage>98</lpage>. <pub-id pub-id-type="doi">10.1016/j.brainres.2009.03.072</pub-id><pub-id pub-id-type="pmid">19450569</pub-id></mixed-citation></ref><ref id="B126"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Paschos</surname><given-names>G. K.</given-names></name><name><surname>Ibrahim</surname><given-names>S.</given-names></name><name><surname>Song</surname><given-names>W. L.</given-names></name><name><surname>Kunieda</surname><given-names>T.</given-names></name><name><surname>Grant</surname><given-names>G.</given-names></name><name><surname>Reyes</surname><given-names>T. M.</given-names></name><etal></etal></person-group>. (<year>2012</year>). <article-title>Obesity in mice with adipocyte-specific deletion of clock component Arntl</article-title>. <source>Nat. Med</source>. <volume>18</volume>, <fpage>1768</fpage>–<lpage>1777</lpage>. <pub-id pub-id-type="doi">10.1038/nm.2979</pub-id><pub-id pub-id-type="pmid">23142819</pub-id></mixed-citation></ref><ref id="B127"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Patacchioli</surname><given-names>F. R.</given-names></name><name><surname>Monnazzi</surname><given-names>P.</given-names></name><name><surname>Scontrini</surname><given-names>A.</given-names></name><name><surname>Tremante</surname><given-names>E.</given-names></name><name><surname>Caridi</surname><given-names>I.</given-names></name><name><surname>Brunetti</surname><given-names>E.</given-names></name><etal></etal></person-group>. (<year>2003</year>). <article-title>Adrenal dysregulation in amyotrophic lateral sclerosis</article-title>. <source>J. Endocrinol. Invest</source>. <volume>26</volume>, <fpage>RC23</fpage>–<lpage>RC25</lpage>. <pub-id pub-id-type="doi">10.1007/BF03349149</pub-id><pub-id pub-id-type="pmid">15055464</pub-id></mixed-citation></ref><ref id="B128"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Patel</surname><given-names>D. D.</given-names></name><name><surname>Knight</surname><given-names>B. L.</given-names></name><name><surname>Wiggins</surname><given-names>D.</given-names></name><name><surname>Humphreys</surname><given-names>S. M.</given-names></name><name><surname>Gibbons</surname><given-names>G. F.</given-names></name></person-group> (<year>2001</year>). <article-title>Disturbances in the normal regulation of SREBP-sensitive genes in PPAR alpha-deficient mice</article-title>. <source>J. Lipid Res</source>. <volume>42</volume>, <fpage>328</fpage>–<lpage>337</lpage>. <pub-id pub-id-type="pmid">11254743</pub-id></mixed-citation></ref><ref id="B129"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pinto</surname><given-names>C.</given-names></name><name><surname>Cardenas</surname><given-names>P.</given-names></name><name><surname>Osses</surname><given-names>N.</given-names></name><name><surname>Henriquez</surname><given-names>J. P.</given-names></name></person-group> (<year>2013</year>). <article-title>Characterization of Wnt/beta-catenin and BMP/Smad signaling pathways in an <italic>in vitro</italic> model of amyotrophic lateral sclerosis</article-title>. <source>Front. Cell. Neurosci</source>. <volume>7</volume>:<issue>239</issue>. <pub-id pub-id-type="doi">10.3389/fncel.2013.00239</pub-id><pub-id pub-id-type="pmid">24348333</pub-id></mixed-citation></ref><ref id="B130"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Postuma</surname><given-names>R. B.</given-names></name><name><surname>Montplaisir</surname><given-names>J.</given-names></name></person-group> (<year>2009</year>). <article-title>Predicting Parkinson's disease - why, when, and how?</article-title><source>Parkinsonism Relat. Disord</source>. <volume>15</volume>(<issue>Suppl. 3</issue>), <fpage>S105</fpage>–<lpage>S109</lpage>. <pub-id pub-id-type="doi">10.1016/S1353-8020(09)70793-X</pub-id><pub-id pub-id-type="pmid">20082967</pub-id></mixed-citation></ref><ref id="B131"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Preitner</surname><given-names>N.</given-names></name><name><surname>Damiola</surname><given-names>F.</given-names></name><name><surname>Lopez-Molina</surname><given-names>L.</given-names></name><name><surname>Zakany</surname><given-names>J.</given-names></name><name><surname>Duboule</surname><given-names>D.</given-names></name><name><surname>Albrecht</surname><given-names>U.</given-names></name><etal></etal></person-group>. (<year>2002</year>). <article-title>The orphan nuclear receptor REV-ERBalpha controls circadian transcription within the positive limb of the mammalian circadian oscillator</article-title>. <source>Cell</source><volume>110</volume>, <fpage>251</fpage>–<lpage>260</lpage>. <pub-id pub-id-type="doi">10.1016/S0092-8674(02)00825-5</pub-id><pub-id pub-id-type="pmid">12150932</pub-id></mixed-citation></ref><ref id="B132"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Prigogine</surname><given-names>I.</given-names></name><name><surname>Nicolis</surname><given-names>G.</given-names></name><name><surname>Babloyantz</surname><given-names>A.</given-names></name></person-group> (<year>1974</year>). <article-title>Nonequilibrium problems in biological phenomena</article-title>. <source>Ann. N.Y. Acad. Sci</source>. <volume>231</volume>, <fpage>99</fpage>–<lpage>105</lpage>. <pub-id pub-id-type="doi">10.1111/j.1749-6632.1974.tb20557.x</pub-id><pub-id pub-id-type="pmid">4522899</pub-id></mixed-citation></ref><ref id="B133"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Rawadi</surname><given-names>G.</given-names></name><name><surname>Roman-Roman</surname><given-names>S.</given-names></name></person-group> (<year>2005</year>). <article-title>Wnt signalling pathway: a new target for the treatment of osteoporosis</article-title>. <source>Expert Opin. Ther. Targets</source><volume>9</volume>, <fpage>1063</fpage>–<lpage>1077</lpage>. <pub-id pub-id-type="doi">10.1517/14728222.9.5.1063</pub-id><pub-id pub-id-type="pmid">16185158</pub-id></mixed-citation></ref><ref id="B134"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Razeghi</surname><given-names>P.</given-names></name><name><surname>Young</surname><given-names>M. E.</given-names></name><name><surname>Abbasi</surname><given-names>S.</given-names></name><name><surname>Taegtmeyer</surname><given-names>H.</given-names></name></person-group> (<year>2001</year>). <article-title>Hypoxia <italic>in vivo</italic> decreases peroxisome proliferator-activated receptor alpha-regulated gene expression in rat heart</article-title>. <source>Biochem. Biophys. Res. Commun</source>. <volume>287</volume>, <fpage>5</fpage>–<lpage>10</lpage>. <pub-id pub-id-type="doi">10.1006/bbrc.2001.5541</pub-id><pub-id pub-id-type="pmid">11549245</pub-id></mixed-citation></ref><ref id="B135"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Reppert</surname><given-names>S. M.</given-names></name><name><surname>Weaver</surname><given-names>D. R.</given-names></name></person-group> (<year>2001</year>). <article-title>Molecular analysis of mammalian circadian rhythms</article-title>. <source>Annu. Rev. Physiol</source>. <volume>63</volume>, <fpage>647</fpage>–<lpage>676</lpage>. <pub-id pub-id-type="doi">10.1146/annurev.physiol.63.1.647</pub-id><pub-id pub-id-type="pmid">11181971</pub-id></mixed-citation></ref><ref id="B136"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Reppert</surname><given-names>S. M.</given-names></name><name><surname>Weaver</surname><given-names>D. R.</given-names></name></person-group> (<year>2002</year>). <article-title>Coordination of circadian timing in mammals</article-title>. <source>Nature</source><volume>418</volume>, <fpage>935</fpage>–<lpage>941</lpage>. <pub-id pub-id-type="doi">10.1038/nature00965</pub-id><pub-id pub-id-type="pmid">12198538</pub-id></mixed-citation></ref><ref id="B137"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Richardson</surname><given-names>P.</given-names></name><name><surname>McKenna</surname><given-names>W.</given-names></name><name><surname>Bristow</surname><given-names>M.</given-names></name><name><surname>Maisch</surname><given-names>B.</given-names></name><name><surname>Mautner</surname><given-names>B.</given-names></name><name><surname>O'Connell</surname><given-names>J.</given-names></name><etal></etal></person-group>. (<year>1996</year>). <article-title>Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of cardiomyopathies</article-title>. <source>Circulation</source><volume>93</volume>, <fpage>841</fpage>–<lpage>842</lpage>. <pub-id pub-id-type="doi">10.1161/01.CIR.93.5.841</pub-id><pub-id pub-id-type="pmid">8598070</pub-id></mixed-citation></ref><ref id="B138"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ross</surname><given-names>O. A.</given-names></name><name><surname>Rutherford</surname><given-names>N. J.</given-names></name><name><surname>Baker</surname><given-names>M.</given-names></name><name><surname>Soto-Ortolaza</surname><given-names>A. I.</given-names></name><name><surname>Carrasquillo</surname><given-names>M. M.</given-names></name><name><surname>DeJesus-Hernandez</surname><given-names>M.</given-names></name><etal></etal></person-group>. (<year>2011</year>). <article-title>Ataxin-2 repeat-length variation and neurodegeneration</article-title>. <source>Hum. Mol. Genet</source>. <volume>20</volume>, <fpage>3207</fpage>–<lpage>3212</lpage>. <pub-id pub-id-type="doi">10.1093/hmg/ddr227</pub-id><pub-id pub-id-type="pmid">21610160</pub-id></mixed-citation></ref><ref id="B139"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ross</surname><given-names>S. E.</given-names></name><name><surname>Hemati</surname><given-names>N.</given-names></name><name><surname>Longo</surname><given-names>K. A.</given-names></name><name><surname>Bennett</surname><given-names>C. N.</given-names></name><name><surname>Lucas</surname><given-names>P. C.</given-names></name><name><surname>Erickson</surname><given-names>R. L.</given-names></name><etal></etal></person-group>. (<year>2000</year>). <article-title>Inhibition of adipogenesis by Wnt signaling</article-title>. <source>Science</source><volume>289</volume>, <fpage>950</fpage>–<lpage>953</lpage>. <pub-id pub-id-type="doi">10.1126/science.289.5481.950</pub-id><pub-id pub-id-type="pmid">10937998</pub-id></mixed-citation></ref><ref id="B140"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Rudic</surname><given-names>R. D.</given-names></name><name><surname>Fulton</surname><given-names>D. J.</given-names></name></person-group> (<year>2009</year>). <article-title>Pressed for time: the circadian clock and hypertension</article-title>. <source>J. Appl. Physiol</source>. <volume>107</volume>, <fpage>1328</fpage>–<lpage>1338</lpage>. <pub-id pub-id-type="doi">10.1152/japplphysiol.00661.2009</pub-id><pub-id pub-id-type="pmid">19679741</pub-id></mixed-citation></ref><ref id="B141"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ryan</surname><given-names>M. J.</given-names></name><name><surname>Didion</surname><given-names>S. P.</given-names></name><name><surname>Mathur</surname><given-names>S.</given-names></name><name><surname>Faraci</surname><given-names>F. M.</given-names></name><name><surname>Sigmund</surname><given-names>C. D.</given-names></name></person-group> (<year>2004</year>). <article-title>PPAR(gamma) agonist rosiglitazone improves vascular function and lowers blood pressure in hypertensive transgenic mice</article-title>. <source>Hypertension</source><volume>43</volume>, <fpage>661</fpage>–<lpage>666</lpage>. <pub-id pub-id-type="doi">10.1161/01.HYP.0000116303.71408.c2</pub-id><pub-id pub-id-type="pmid">14744930</pub-id></mixed-citation></ref><ref id="B142"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sakai</surname><given-names>T.</given-names></name><name><surname>Tamura</surname><given-names>T.</given-names></name><name><surname>Kitamoto</surname><given-names>T.</given-names></name><name><surname>Kidokoro</surname><given-names>Y.</given-names></name></person-group> (<year>2004</year>). <article-title>A clock gene, period, plays a key role in long-term memory formation in Drosophila</article-title>. <source>Proc. Natl. Acad. Sci. U.S.A</source>. <volume>101</volume>, <fpage>16058</fpage>–<lpage>16063</lpage>. <pub-id pub-id-type="doi">10.1073/pnas.0401472101</pub-id><pub-id pub-id-type="pmid">15522971</pub-id></mixed-citation></ref><ref id="B143"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sarraf</surname><given-names>P.</given-names></name><name><surname>Mueller</surname><given-names>E.</given-names></name><name><surname>Smith</surname><given-names>W. M.</given-names></name><name><surname>Wright</surname><given-names>H. M.</given-names></name><name><surname>Kum</surname><given-names>J. B.</given-names></name><name><surname>Aaltonen</surname><given-names>L. A.</given-names></name><etal></etal></person-group>. (<year>1999</year>). <article-title>Loss-of-function mutations in PPAR gamma associated with human colon cancer</article-title>. <source>Mol. Cell</source><volume>3</volume>, <fpage>799</fpage>–<lpage>804</lpage>. <pub-id pub-id-type="doi">10.1016/S1097-2765(01)80012-5</pub-id><pub-id pub-id-type="pmid">10394368</pub-id></mixed-citation></ref><ref id="B144"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Savvidis</surname><given-names>C.</given-names></name><name><surname>Koutsilieris</surname><given-names>M.</given-names></name></person-group> (<year>2012</year>). <article-title>Circadian rhythm disruption in cancer biology</article-title>. <source>Mol. Med</source>. <volume>18</volume>, <fpage>1249</fpage>–<lpage>1260</lpage>. <pub-id pub-id-type="doi">10.2119/molmed.2012.00077</pub-id><pub-id pub-id-type="pmid">22811066</pub-id></mixed-citation></ref><ref id="B145"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Schibler</surname><given-names>U.</given-names></name><name><surname>Sassone-Corsi</surname><given-names>P.</given-names></name></person-group> (<year>2002</year>). <article-title>A web of circadian pacemakers</article-title>. <source>Cell</source><volume>111</volume>, <fpage>919</fpage>–<lpage>922</lpage>. <pub-id pub-id-type="doi">10.1016/S0092-8674(02)01225-4</pub-id><pub-id pub-id-type="pmid">12507418</pub-id></mixed-citation></ref><ref id="B146"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Schintu</surname><given-names>N.</given-names></name><name><surname>Frau</surname><given-names>L.</given-names></name><name><surname>Ibba</surname><given-names>M.</given-names></name><name><surname>Caboni</surname><given-names>P.</given-names></name><name><surname>Garau</surname><given-names>A.</given-names></name><name><surname>Carboni</surname><given-names>E.</given-names></name><etal></etal></person-group>. (<year>2009</year>). <article-title>PPAR-gamma-mediated neuroprotection in a chronic mouse model of Parkinson's disease</article-title>. <source>Eur. J. Neurosci</source>. <volume>29</volume>, <fpage>954</fpage>–<lpage>963</lpage>. <pub-id pub-id-type="doi">10.1111/j.1460-9568.2009.06657.x</pub-id><pub-id pub-id-type="pmid">19245367</pub-id></mixed-citation></ref><ref id="B147"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Schroeder</surname><given-names>A. M.</given-names></name><name><surname>Loh</surname><given-names>D. H.</given-names></name><name><surname>Jordan</surname><given-names>M. C.</given-names></name><name><surname>Roos</surname><given-names>K. P.</given-names></name><name><surname>Colwell</surname><given-names>C. S.</given-names></name></person-group> (<year>2011</year>). <article-title>Baroreceptor reflex dysfunction in the BACHD mouse model of Huntington's disease</article-title>. <source>PLoS Curr</source><volume>3</volume>:<fpage>RRN1266</fpage>. <pub-id pub-id-type="doi">10.1371/currents.RRN1266</pub-id><pub-id pub-id-type="pmid">22069044</pub-id></mixed-citation></ref><ref id="B148"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sen-Chowdhry</surname><given-names>S.</given-names></name><name><surname>Syrris</surname><given-names>P.</given-names></name><name><surname>McKenna</surname><given-names>W. J.</given-names></name></person-group> (<year>2005</year>). <article-title>Genetics of right ventricular cardiomyopathy</article-title>. <source>J. Cardiovasc. Electrophysiol</source>. <volume>16</volume>, <fpage>927</fpage>–<lpage>935</lpage>. <pub-id pub-id-type="doi">10.1111/j.1540-8167.2005.40842.x</pub-id><pub-id pub-id-type="pmid">16101641</pub-id></mixed-citation></ref><ref id="B149"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shirai</surname><given-names>H.</given-names></name><name><surname>Oishi</surname><given-names>K.</given-names></name><name><surname>Kudo</surname><given-names>T.</given-names></name><name><surname>Shibata</surname><given-names>S.</given-names></name><name><surname>Ishida</surname><given-names>N.</given-names></name></person-group> (<year>2007</year>). <article-title>PPARalpha is a potential therapeutic target of drugs to treat circadian rhythm sleep disorders</article-title>. <source>Biochem. Biophys. Res. Commun</source>. <volume>357</volume>, <fpage>679</fpage>–<lpage>682</lpage>. <pub-id pub-id-type="doi">10.1016/j.bbrc.2007.04.002</pub-id><pub-id pub-id-type="pmid">17449013</pub-id></mixed-citation></ref><ref id="B150"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Singh</surname><given-names>K. K.</given-names></name></person-group> (<year>2013</year>). <article-title>An emerging role for Wnt and GSK3 signaling pathways in schizophrenia</article-title>. <source>Clin. Genet</source>. <volume>83</volume>, <fpage>511</fpage>–<lpage>517</lpage>. <pub-id pub-id-type="doi">10.1111/cge.12111</pub-id><pub-id pub-id-type="pmid">23379509</pub-id></mixed-citation></ref><ref id="B151"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sinha</surname><given-names>D.</given-names></name><name><surname>Wang</surname><given-names>Z.</given-names></name><name><surname>Ruchalski</surname><given-names>K. L.</given-names></name><name><surname>Levine</surname><given-names>J. S.</given-names></name><name><surname>Krishnan</surname><given-names>S.</given-names></name><name><surname>Lieberthal</surname><given-names>W.</given-names></name><etal></etal></person-group>. (<year>2005</year>). <article-title>Lithium activates the Wnt and phosphatidylinositol 3-kinase Akt signaling pathways to promote cell survival in the absence of soluble survival factors</article-title>. <source>Am. J. Physiol. Renal Physiol</source>. <volume>288</volume>, <fpage>F703</fpage>–<lpage>F713</lpage>. <pub-id pub-id-type="doi">10.1152/ajprenal.00189.2004</pub-id><pub-id pub-id-type="pmid">15572521</pub-id></mixed-citation></ref><ref id="B152"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Stampfer</surname><given-names>M. J.</given-names></name></person-group> (<year>2006</year>). <article-title>Cardiovascular disease and Alzheimer's disease: common links</article-title>. <source>J. Intern. Med</source>. <volume>260</volume>, <fpage>211</fpage>–<lpage>223</lpage>. <pub-id pub-id-type="doi">10.1111/j.1365-2796.2006.01687.x</pub-id><pub-id pub-id-type="pmid">16918818</pub-id></mixed-citation></ref><ref id="B153"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Storch</surname><given-names>K. F.</given-names></name><name><surname>Lipan</surname><given-names>O.</given-names></name><name><surname>Leykin</surname><given-names>I.</given-names></name><name><surname>Viswanathan</surname><given-names>N.</given-names></name><name><surname>Davis</surname><given-names>F. C.</given-names></name><name><surname>Wong</surname><given-names>W. H.</given-names></name><etal></etal></person-group>. (<year>2002</year>). <article-title>Extensive and divergent circadian gene expression in liver and heart</article-title>. <source>Nature</source><volume>417</volume>, <fpage>78</fpage>–<lpage>83</lpage>. <pub-id pub-id-type="doi">10.1038/nature744</pub-id><pub-id pub-id-type="pmid">11967526</pub-id></mixed-citation></ref><ref id="B154"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sugawara</surname><given-names>A.</given-names></name><name><surname>Uruno</surname><given-names>A.</given-names></name><name><surname>Kudo</surname><given-names>M.</given-names></name><name><surname>Matsuda</surname><given-names>K.</given-names></name><name><surname>Yang</surname><given-names>C. W.</given-names></name><name><surname>Ito</surname><given-names>S.</given-names></name></person-group> (<year>2010</year>). <article-title>Effects of PPARgamma on hypertension, atherosclerosis, and chronic kidney disease</article-title>. <source>Endocr. J</source>. <volume>57</volume>, <fpage>847</fpage>–<lpage>852</lpage>. <pub-id pub-id-type="doi">10.1507/endocrj.K10E-281</pub-id><pub-id pub-id-type="pmid">20890053</pub-id></mixed-citation></ref><ref id="B155"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Swanson</surname><given-names>C. R.</given-names></name><name><surname>Joers</surname><given-names>V.</given-names></name><name><surname>Bondarenko</surname><given-names>V.</given-names></name><name><surname>Brunner</surname><given-names>K.</given-names></name><name><surname>Simmons</surname><given-names>H. A.</given-names></name><name><surname>Ziegler</surname><given-names>T. E.</given-names></name><etal></etal></person-group>. (<year>2011</year>). <article-title>The PPAR-gamma agonist pioglitazone modulates inflammation and induces neuroprotection in parkinsonian monkeys</article-title>. <source>J. Neuroinflammation</source><volume>8</volume>:<fpage>91</fpage>. <pub-id pub-id-type="doi">10.1186/1742-2094-8-91</pub-id><pub-id pub-id-type="pmid">21819568</pub-id></mixed-citation></ref><ref id="B156"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Swartz</surname><given-names>H. A.</given-names></name><name><surname>Fagiolini</surname><given-names>A.</given-names></name></person-group> (<year>2012</year>). <article-title>Cardiovascular disease and bipolar disorder: risk and clinical implications</article-title>. <source>J. Clin. Psychiatry</source><volume>73</volume>, <fpage>1563</fpage>–<lpage>1565</lpage>. <pub-id pub-id-type="doi">10.4088/JCP.12ac08227</pub-id><pub-id pub-id-type="pmid">23290329</pub-id></mixed-citation></ref><ref id="B157"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Takada</surname><given-names>I.</given-names></name><name><surname>Kouzmenko</surname><given-names>A. P.</given-names></name><name><surname>Kato</surname><given-names>S.</given-names></name></person-group> (<year>2009</year>). <article-title>Wnt and PPARgamma signaling in osteoblastogenesis and adipogenesis</article-title>. <source>Nat. Rev. Rheumatol</source>. <volume>5</volume>, <fpage>442</fpage>–<lpage>447</lpage>. <pub-id pub-id-type="doi">10.1038/nrrheum.2009.137</pub-id><pub-id pub-id-type="pmid">19581903</pub-id></mixed-citation></ref><ref id="B158"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Takeda</surname><given-names>N.</given-names></name><name><surname>Maemura</surname><given-names>K.</given-names></name></person-group> (<year>2011</year>). <article-title>Circadian clock and cardiovascular disease</article-title>. <source>J. Cardiol</source>. <volume>57</volume>, <fpage>249</fpage>–<lpage>256</lpage>. <pub-id pub-id-type="doi">10.1016/j.jjcc.2011.02.006</pub-id><pub-id pub-id-type="pmid">21441015</pub-id></mixed-citation></ref><ref id="B159"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Takeda</surname><given-names>N.</given-names></name><name><surname>Maemura</surname><given-names>K.</given-names></name><name><surname>Horie</surname><given-names>S.</given-names></name><name><surname>Oishi</surname><given-names>K.</given-names></name><name><surname>Imai</surname><given-names>Y.</given-names></name><name><surname>Harada</surname><given-names>T.</given-names></name><etal></etal></person-group>. (<year>2007</year>). <article-title>Thrombomodulin is a clock-controlled gene in vascular endothelial cells</article-title>. <source>J. Biol. Chem</source>. <volume>282</volume>, <fpage>32561</fpage>–<lpage>32567</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.M705692200</pub-id><pub-id pub-id-type="pmid">17848551</pub-id></mixed-citation></ref><ref id="B160"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tougas</surname><given-names>G.</given-names></name></person-group> (<year>2000</year>). <article-title>The autonomic nervous system in functional bowel disorders</article-title>. <source>Gut</source><volume>47</volume>(<issue>Suppl. 4</issue>), <fpage>iv78</fpage>–<lpage>iv80</lpage>. discussion: iv87. <pub-id pub-id-type="pmid">11076926</pub-id></mixed-citation></ref><ref id="B161"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ueda</surname><given-names>H. R.</given-names></name><name><surname>Chen</surname><given-names>W.</given-names></name><name><surname>Adachi</surname><given-names>A.</given-names></name><name><surname>Wakamatsu</surname><given-names>H.</given-names></name><name><surname>Hayashi</surname><given-names>S.</given-names></name><name><surname>Takasugi</surname><given-names>T.</given-names></name><etal></etal></person-group>. (<year>2002</year>). <article-title>A transcription factor response element for gene expression during circadian night</article-title>. <source>Nature</source><volume>418</volume>, <fpage>534</fpage>–<lpage>539</lpage>. <pub-id pub-id-type="doi">10.1038/nature00906</pub-id><pub-id pub-id-type="pmid">12152080</pub-id></mixed-citation></ref><ref id="B162"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Valvezan</surname><given-names>A. J.</given-names></name><name><surname>Klein</surname><given-names>P. S.</given-names></name></person-group> (<year>2012</year>). <article-title>GSK-3 and Wnt signaling in neurogenesis and bipolar disorder</article-title>. <source>Front. Mol. Neurosci</source>. <volume>5</volume>:<issue>1</issue>. <pub-id pub-id-type="doi">10.3389/fnmol.2012.00001</pub-id><pub-id pub-id-type="pmid">22319467</pub-id></mixed-citation></ref><ref id="B163"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Viola</surname><given-names>A. U.</given-names></name><name><surname>James</surname><given-names>L. M.</given-names></name><name><surname>Archer</surname><given-names>S. N.</given-names></name><name><surname>Dijk</surname><given-names>D. J.</given-names></name></person-group> (<year>2008</year>). <article-title>PER3 polymorphism and cardiac autonomic control: effects of sleep debt and circadian phase</article-title>. <source>Am. J. Physiol. Heart Circ. Physiol</source>. <volume>295</volume>, <fpage>H2156</fpage>–<lpage>H2163</lpage>. <pub-id pub-id-type="doi">10.1152/ajpheart.00662.2008</pub-id><pub-id pub-id-type="pmid">18835917</pub-id></mixed-citation></ref><ref id="B164"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Virag</surname><given-names>J. A.</given-names></name><name><surname>Anderson</surname><given-names>E. J.</given-names></name><name><surname>Kent</surname><given-names>S. D.</given-names></name><name><surname>Blanton</surname><given-names>H. D.</given-names></name><name><surname>Johnson</surname><given-names>T. L.</given-names></name><name><surname>Moukdar</surname><given-names>F.</given-names></name><etal></etal></person-group>. (<year>2013</year>). <article-title>Cardioprotection via preserved mitochondrial structure and function in the mPer2-mutant mouse myocardium</article-title>. <source>Am. J. Physiol. Heart Circ. Physiol</source>. <volume>305</volume>, <fpage>H477</fpage>–<lpage>H483</lpage>. <pub-id pub-id-type="doi">10.1152/ajpheart.00914.2012</pub-id><pub-id pub-id-type="pmid">23771689</pub-id></mixed-citation></ref><ref id="B165"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Walker</surname><given-names>F. O.</given-names></name></person-group> (<year>2007</year>). <article-title>Huntington's disease</article-title>. <source>Lancet</source><volume>369</volume>, <fpage>218</fpage>–<lpage>228</lpage>. <pub-id pub-id-type="doi">10.1016/S0140-6736(07)60111-1</pub-id><pub-id pub-id-type="pmid">17240289</pub-id></mixed-citation></ref><ref id="B166"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wan</surname><given-names>W.</given-names></name><name><surname>Xia</surname><given-names>S.</given-names></name><name><surname>Kalionis</surname><given-names>B.</given-names></name><name><surname>Liu</surname><given-names>L.</given-names></name><name><surname>Li</surname><given-names>Y.</given-names></name></person-group> (<year>2014</year>). <article-title>The role of Wnt signaling in the development of Alzheimer's disease: a potential therapeutic target?</article-title><source>Biomed. Res. Int</source>. <volume>2014</volume>:<fpage>301575</fpage>. <pub-id pub-id-type="doi">10.1155/2014/301575</pub-id><pub-id pub-id-type="pmid">24883305</pub-id></mixed-citation></ref><ref id="B167"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wan</surname><given-names>Y.</given-names></name><name><surname>Chong</surname><given-names>L. W.</given-names></name><name><surname>Evans</surname><given-names>R. M.</given-names></name></person-group> (<year>2007</year>). <article-title>PPAR-gamma regulates osteoclastogenesis in mice</article-title>. <source>Nat. Med</source>. <volume>13</volume>, <fpage>1496</fpage>–<lpage>1503</lpage>. <pub-id pub-id-type="doi">10.1038/nm1672</pub-id><pub-id pub-id-type="pmid">18059282</pub-id></mixed-citation></ref><ref id="B168"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wang</surname><given-names>J.</given-names></name><name><surname>Yin</surname><given-names>L.</given-names></name><name><surname>Lazar</surname><given-names>M. A.</given-names></name></person-group> (<year>2006</year>). <article-title>The orphan nuclear receptor Rev-erb alpha regulates circadian expression of plasminogen activator inhibitor type 1</article-title>. <source>J. Biol. Chem</source>. <volume>281</volume>, <fpage>33842</fpage>–<lpage>33848</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.M607873200</pub-id><pub-id pub-id-type="pmid">16968709</pub-id></mixed-citation></ref><ref id="B169"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wang</surname><given-names>N.</given-names></name><name><surname>Yang</surname><given-names>G.</given-names></name><name><surname>Jia</surname><given-names>Z.</given-names></name><name><surname>Zhang</surname><given-names>H.</given-names></name><name><surname>Aoyagi</surname><given-names>T.</given-names></name><name><surname>Soodvilai</surname><given-names>S.</given-names></name><etal></etal></person-group>. (<year>2008</year>). <article-title>Vascular PPARgamma controls circadian variation in blood pressure and heart rate through Bmal1</article-title>. <source>Cell Metab</source>. <volume>8</volume>, <fpage>482</fpage>–<lpage>491</lpage>. <pub-id pub-id-type="doi">10.1016/j.cmet.2008.10.009</pub-id><pub-id pub-id-type="pmid">19041764</pub-id></mixed-citation></ref><ref id="B170"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Xiao</surname><given-names>Y.</given-names></name><name><surname>Mou</surname><given-names>Y.</given-names></name><name><surname>Zhao</surname><given-names>Y.</given-names></name><name><surname>Blankesteijn</surname><given-names>W. M.</given-names></name><name><surname>Hall</surname><given-names>J. L.</given-names></name></person-group> (<year>2002</year>). <article-title>A role for the beta-catenin/T-cell factor signaling cascade in vascular remodeling</article-title>. <source>Circ. Res</source>. <volume>90</volume>, <fpage>340</fpage>–<lpage>347</lpage>. <pub-id pub-id-type="doi">10.1161/hh0302.104466</pub-id><pub-id pub-id-type="pmid">11861424</pub-id></mixed-citation></ref><ref id="B171"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Weaver</surname><given-names>D. R.</given-names></name></person-group> (<year>1998</year>). <article-title>The suprachiasmatic nucleus: a 25-year retrospective</article-title>. <source>J. Biol. Rhythms</source><volume>13</volume>, <fpage>100</fpage>–<lpage>112</lpage>. <pub-id pub-id-type="doi">10.1177/074873098128999952</pub-id><pub-id pub-id-type="pmid">9554572</pub-id></mixed-citation></ref><ref id="B172"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Woon</surname><given-names>P. Y.</given-names></name><name><surname>Kaisaki</surname><given-names>P. J.</given-names></name><name><surname>Braganca</surname><given-names>J.</given-names></name><name><surname>Bihoreau</surname><given-names>M. T.</given-names></name><name><surname>Levy</surname><given-names>J. C.</given-names></name><name><surname>Farrall</surname><given-names>M.</given-names></name><etal></etal></person-group>. (<year>2007</year>). <article-title>Aryl hydrocarbon receptor nuclear translocator-like (BMAL1) is associated with susceptibility to hypertension and type 2 diabetes</article-title>. <source>Proc. Natl. Acad. Sci. U.S.A</source>. <volume>104</volume>, <fpage>14412</fpage>–<lpage>14417</lpage>. <pub-id pub-id-type="doi">10.1073/pnas.0703247104</pub-id><pub-id pub-id-type="pmid">17728404</pub-id></mixed-citation></ref><ref id="B173"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wu</surname><given-names>X.</given-names></name><name><surname>Liu</surname><given-names>Z.</given-names></name><name><surname>Shi</surname><given-names>G.</given-names></name><name><surname>Xing</surname><given-names>L.</given-names></name><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Gu</surname><given-names>X.</given-names></name><etal></etal></person-group>. (<year>2011</year>). <article-title>The circadian clock influences heart performance</article-title>. <source>J. Biol. Rhythms</source><volume>26</volume>, <fpage>402</fpage>–<lpage>411</lpage>. <pub-id pub-id-type="doi">10.1177/0748730411414168</pub-id><pub-id pub-id-type="pmid">21921294</pub-id></mixed-citation></ref><ref id="B174"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wulff</surname><given-names>K.</given-names></name><name><surname>Dijk</surname><given-names>D. J.</given-names></name><name><surname>Middleton</surname><given-names>B.</given-names></name><name><surname>Foster</surname><given-names>R. G.</given-names></name><name><surname>Joyce</surname><given-names>E. M.</given-names></name></person-group> (<year>2012</year>). <article-title>Sleep and circadian rhythm disruption in schizophrenia</article-title>. <source>Br. J. Psychiatry</source><volume>200</volume>, <fpage>308</fpage>–<lpage>316</lpage>. <pub-id pub-id-type="doi">10.1192/bjp.bp.111.096321</pub-id><pub-id pub-id-type="pmid">22194182</pub-id></mixed-citation></ref><ref id="B175"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>G.</given-names></name><name><surname>Jia</surname><given-names>Z.</given-names></name><name><surname>Aoyagi</surname><given-names>T.</given-names></name><name><surname>McClain</surname><given-names>D.</given-names></name><name><surname>Mortensen</surname><given-names>R. M.</given-names></name><name><surname>Yang</surname><given-names>T.</given-names></name></person-group> (<year>2012</year>). <article-title>Systemic PPARgamma deletion impairs circadian rhythms of behavior and metabolism</article-title>. <source>PLoS ONE</source><volume>7</volume>:<fpage>e38117</fpage>. <pub-id pub-id-type="doi">10.1371/journal.pone.0038117</pub-id><pub-id pub-id-type="pmid">22899986</pub-id></mixed-citation></ref><ref id="B176"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>T.</given-names></name><name><surname>Aoyagi</surname><given-names>T.</given-names></name><name><surname>Dowtown</surname><given-names>M.</given-names></name><name><surname>Liu</surname><given-names>M.</given-names></name><name><surname>Whitehead</surname><given-names>K.</given-names></name><name><surname>Jia</surname><given-names>Z.</given-names></name></person-group> (<year>2013</year>). <article-title>Whole-body deletion of PPAR in mice increases sympathetic nerve activity</article-title>. <source>Circulation</source><volume>62</volume>:<fpage>A399</fpage>.</mixed-citation></ref><ref id="B177"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>X.</given-names></name><name><surname>Downes</surname><given-names>M.</given-names></name><name><surname>Yu</surname><given-names>R. T.</given-names></name><name><surname>Bookout</surname><given-names>A. L.</given-names></name><name><surname>He</surname><given-names>W.</given-names></name><name><surname>Straume</surname><given-names>M.</given-names></name><etal></etal></person-group>. (<year>2006</year>). <article-title>Nuclear receptor expression links the circadian clock to metabolism</article-title>. <source>Cell</source><volume>126</volume>, <fpage>801</fpage>–<lpage>810</lpage>. <pub-id pub-id-type="doi">10.1016/j.cell.2006.06.050</pub-id><pub-id pub-id-type="pmid">16923398</pub-id></mixed-citation></ref><ref id="B178"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>Y.</given-names></name></person-group> (<year>2012</year>). <article-title>Wnt signaling in development and disease</article-title>. <source>Cell Biosci</source>. <volume>2</volume>:<fpage>14</fpage>. <pub-id pub-id-type="doi">10.1186/2045-3701-2-14</pub-id><pub-id pub-id-type="pmid">22520685</pub-id></mixed-citation></ref><ref id="B179"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yin</surname><given-names>L.</given-names></name><name><surname>Wang</surname><given-names>J.</given-names></name><name><surname>Klein</surname><given-names>P. S.</given-names></name><name><surname>Lazar</surname><given-names>M. A.</given-names></name></person-group> (<year>2006</year>). <article-title>Nuclear receptor Rev-erbalpha is a critical lithium-sensitive component of the circadian clock</article-title>. <source>Science</source><volume>311</volume>, <fpage>1002</fpage>–<lpage>1005</lpage>. <pub-id pub-id-type="doi">10.1126/science.1121613</pub-id><pub-id pub-id-type="pmid">16484495</pub-id></mixed-citation></ref><ref id="B180"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Young</surname><given-names>M. E.</given-names></name></person-group> (<year>2009</year>). <article-title>Anticipating anticipation: pursuing identification of cardiomyocyte circadian clock function</article-title>. <source>J. Appl. Physiol</source>. <volume>107</volume>, <fpage>1339</fpage>–<lpage>1347</lpage>. <pub-id pub-id-type="doi">10.1152/japplphysiol.00473.2009</pub-id><pub-id pub-id-type="pmid">19608929</pub-id></mixed-citation></ref><ref id="B181"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Young</surname><given-names>M. E.</given-names></name><name><surname>Laws</surname><given-names>F. A.</given-names></name><name><surname>Goodwin</surname><given-names>G. W.</given-names></name><name><surname>Taegtmeyer</surname><given-names>H.</given-names></name></person-group> (<year>2001a</year>). <article-title>Reactivation of peroxisome proliferator-activated receptor alpha is associated with contractile dysfunction in hypertrophied rat heart</article-title>. <source>J. Biol. Chem</source>. <volume>276</volume>, <fpage>44390</fpage>–<lpage>44395</lpage>. <pub-id pub-id-type="doi">10.1074/jbc.M103826200</pub-id><pub-id pub-id-type="pmid">11574533</pub-id></mixed-citation></ref><ref id="B182"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Young</surname><given-names>M. E.</given-names></name><name><surname>Razeghi</surname><given-names>P.</given-names></name><name><surname>Cedars</surname><given-names>A. M.</given-names></name><name><surname>Guthrie</surname><given-names>P. H.</given-names></name><name><surname>Taegtmeyer</surname><given-names>H.</given-names></name></person-group> (<year>2001b</year>). <article-title>Intrinsic diurnal variations in cardiac metabolism and contractile function</article-title>. <source>Circ. Res</source>. <volume>89</volume>, <fpage>1199</fpage>–<lpage>1208</lpage>. <pub-id pub-id-type="doi">10.1161/hh2401.100741</pub-id><pub-id pub-id-type="pmid">11739286</pub-id></mixed-citation></ref><ref id="B183"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Young</surname><given-names>M. E.</given-names></name><name><surname>Razeghi</surname><given-names>P.</given-names></name><name><surname>Taegtmeyer</surname><given-names>H.</given-names></name></person-group> (<year>2001c</year>). <article-title>Clock genes in the heart: characterization and attenuation with hypertrophy</article-title>. <source>Circ. Res</source>. <volume>88</volume>, <fpage>1142</fpage>–<lpage>1150</lpage>. <pub-id pub-id-type="doi">10.1161/hh1101.091190</pub-id><pub-id pub-id-type="pmid">11397780</pub-id></mixed-citation></ref><ref id="B184"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Young</surname><given-names>M. E.</given-names></name><name><surname>Wilson</surname><given-names>C. R.</given-names></name><name><surname>Razeghi</surname><given-names>P.</given-names></name><name><surname>Guthrie</surname><given-names>P. H.</given-names></name><name><surname>Taegtmeyer</surname><given-names>H.</given-names></name></person-group> (<year>2002</year>). <article-title>Alterations of the circadian clock in the heart by streptozotocin-induced diabetes</article-title>. <source>J. Mol. Cell. Cardiol</source>. <volume>34</volume>, <fpage>223</fpage>–<lpage>231</lpage>. <pub-id pub-id-type="doi">10.1006/jmcc.2001.1504</pub-id><pub-id pub-id-type="pmid">11851361</pub-id></mixed-citation></ref><ref id="B185"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Young</surname><given-names>M. W.</given-names></name><name><surname>Kay</surname><given-names>S. A.</given-names></name></person-group> (<year>2001</year>). <article-title>Time zones: a comparative genetics of circadian clocks</article-title>. <source>Nat. Rev. Genet</source>. <volume>2</volume>, <fpage>702</fpage>–<lpage>715</lpage>. <pub-id pub-id-type="doi">10.1038/35088576</pub-id><pub-id pub-id-type="pmid">11533719</pub-id></mixed-citation></ref><ref id="B186"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yu</surname><given-names>Y.</given-names></name><name><surname>Zhang</surname><given-names>Z. H.</given-names></name><name><surname>Wei</surname><given-names>S. G.</given-names></name><name><surname>Weiss</surname><given-names>R. M.</given-names></name><name><surname>Felder</surname><given-names>R. B.</given-names></name></person-group> (<year>2012</year>). <article-title>Peroxisome proliferator-activated receptor-gamma regulates inflammation and renin-angiotensin system activity in the hypothalamic paraventricular nucleus and ameliorates peripheral manifestations of heart failure</article-title>. <source>Hypertension</source><volume>59</volume>, <fpage>477</fpage>–<lpage>484</lpage>. <pub-id pub-id-type="doi">10.1161/HYPERTENSIONAHA.111.182345</pub-id><pub-id pub-id-type="pmid">22083161</pub-id></mixed-citation></ref><ref id="B187"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yuan</surname><given-names>S.</given-names></name><name><surname>Shi</surname><given-names>Y.</given-names></name><name><surname>Tang</surname><given-names>S. J.</given-names></name></person-group> (<year>2012</year>). <article-title>Wnt signaling in the pathogenesis of multiple sclerosis-associated chronic pain</article-title>. <source>J. Neuroimmune Pharmacol</source>. <volume>7</volume>, <fpage>904</fpage>–<lpage>913</lpage>. <pub-id pub-id-type="doi">10.1007/s11481-012-9370-3</pub-id><pub-id pub-id-type="pmid">22547300</pub-id></mixed-citation></ref><ref id="B188"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yuhara</surname><given-names>H.</given-names></name><name><surname>Steinmaus</surname><given-names>C.</given-names></name><name><surname>Cohen</surname><given-names>S. E.</given-names></name><name><surname>Corley</surname><given-names>D. A.</given-names></name><name><surname>Tei</surname><given-names>Y.</given-names></name><name><surname>Buffler</surname><given-names>P. A.</given-names></name></person-group> (<year>2011</year>). <article-title>Is diabetes mellitus an independent risk factor for colon cancer and rectal cancer?</article-title><source>Am. J. Gastroenterol</source>. <volume>106</volume>, <fpage>1911</fpage>–<lpage>1192</lpage>. <pub-id pub-id-type="doi">10.1038/ajg.2011.301</pub-id><pub-id pub-id-type="pmid">21912438</pub-id></mixed-citation></ref><ref id="B189"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhu</surname><given-names>L.</given-names></name><name><surname>Wang</surname><given-names>Q.</given-names></name><name><surname>Zhang</surname><given-names>L.</given-names></name><name><surname>Fang</surname><given-names>Z.</given-names></name><name><surname>Zhao</surname><given-names>F.</given-names></name><name><surname>Lv</surname><given-names>Z.</given-names></name><etal></etal></person-group>. (<year>2010</year>). <article-title>Hypoxia induces PGC-1alpha expression and mitochondrial biogenesis in the myocardium of TOF patients</article-title>. <source>Cell Res</source>. <volume>20</volume>, <fpage>676</fpage>–<lpage>687</lpage>. <pub-id pub-id-type="doi">10.1038/cr.2010.46</pub-id><pub-id pub-id-type="pmid">20368732</pub-id></mixed-citation></ref><ref id="B190"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhurinsky</surname><given-names>J.</given-names></name><name><surname>Shtutman</surname><given-names>M.</given-names></name><name><surname>Ben-Ze'ev</surname><given-names>A.</given-names></name></person-group> (<year>2000</year>). <article-title>Differential mechanisms of LEF/TCF family-dependent transcriptional activation by beta-catenin and plakoglobin</article-title>. <source>Mol. Cell. Biol</source>. <volume>20</volume>, <fpage>4238</fpage>–<lpage>4252</lpage>. <pub-id pub-id-type="doi">10.1128/MCB.20.12.4238-4252.2000</pub-id><pub-id pub-id-type="pmid">10825188</pub-id></mixed-citation></ref><ref id="B191"><mixed-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zylka</surname><given-names>M. J.</given-names></name><name><surname>Shearman</surname><given-names>L. P.</given-names></name><name><surname>Weaver</surname><given-names>D. R.</given-names></name><name><surname>Reppert</surname><given-names>S. M.</given-names></name></person-group> (<year>1998</year>). <article-title>Three period homologs in mammals: differential light responses in the suprachiasmatic circadian clock and oscillating transcripts outside of brain</article-title>. <source>Neuron</source><volume>20</volume>, <fpage>1103</fpage>–<lpage>1110</lpage>. <pub-id pub-id-type="doi">10.1016/S0896-6273(00)80492-4</pub-id><pub-id pub-id-type="pmid">9655499</pub-id></mixed-citation></ref></ref-list><glossary><def-list><title>Abbreviations</title><def-item><term>CR</term><def><p>circadian rhythm</p></def></def-item><def-item><term>PPAR</term><def><p>Peroxisome proliferator-activated receptor</p></def></def-item><def-item><term>SCN</term><def><p>suprachiasmatic nucleus</p></def></def-item><def-item><term>APC</term><def><p>adenomatous polyposis coli</p></def></def-item><def-item><term>Dsh</term><def><p>Disheveled</p></def></def-item><def-item><term>GSK3-beta</term><def><p>glycogen synthase kinase 3-beta</p></def></def-item><def-item><term>LRP5/6</term><def><p>low density lipoprotein receptor-related protein 5/6</p></def></def-item><def-item><term>Fzd</term><def><p>Frizzled</p></def></def-item><def-item><term>Tcf/Lef</term><def><p>T cell/lymphoid-enhancing binding</p></def></def-item><def-item><term>Clock</term><def><p>Circadian locomotor output cycles kaput</p></def></def-item><def-item><term>Ccm</term><def><p>cardiomyocyte-specific clock mutant</p></def></def-item><def-item><term>FAO</term><def><p>fatty acid oxidation</p></def></def-item><def-item><term>RXR</term><def><p>retinoid X receptor</p></def></def-item><def-item><term>PPRE</term><def><p>peroxisome proliferator response element</p></def></def-item><def-item><term>TZD</term><def><p>thiazolidinedione</p></def></def-item><def-item><term>Bmal1</term><def><p>Brain and muscle aryl-hydrocarbon receptor nuclear translocator-like</p></def></def-item><def-item><term>Cry</term><def><p>cryptochrome</p></def></def-item><def-item><term>Per</term><def><p>Period</p></def></def-item><def-item><term>Ccg</term><def><p>clock-controlled genes</p></def></def-item><def-item><term>Ror</term><def><p>related orphan receptor</p></def></def-item><def-item><term>TZD</term><def><p>thiazolidinediones</p></def></def-item><def-item><term>ARVC</term><def><p>arrhythmogenic right ventricular cardiomyopathy</p></def></def-item><def-item><term>DSG</term><def><p>desmoglein</p></def></def-item><def-item><term>DSC</term><def><p>desmocollin</p></def></def-item><def-item><term>PKP</term><def><p>plakophilin</p></def></def-item><def-item><term>PG</term><def><p>plakoglobin</p></def></def-item><def-item><term>DSP</term><def><p>desmoplakin</p></def></def-item><def-item><term>PDK</term><def><p>pyruvate deshydrogenase kinase</p></def></def-item><def-item><term>HIF1 alpha</term><def><p>hypoxia-inducible factor 1 alpha</p></def></def-item><def-item><term>PGC-1 alpha</term><def><p>PPAR gamma co-activator 1 alpha</p></def></def-item><def-item><term>M-CPT1</term><def><p>muscle carnitine palmitoyltransferase 1</p></def></def-item><def-item><term>ANS</term><def><p>autonomous nervous system</p></def></def-item><def-item><term>AD</term><def><p>Alzheimer Disease</p></def></def-item><def-item><term>HD</term><def><p>Huntington disease</p></def></def-item><def-item><term>ALS</term><def><p>Amyotrophic lateral sclerosis</p></def></def-item><def-item><term>PD</term><def><p>Parkinson disease</p></def></def-item><def-item><term>MS</term><def><p>Multiple sclerosis</p></def></def-item><def-item><term>FRDA</term><def><p>Friedreich ataxia</p></def></def-item><def-item><term>Abeta</term><def><p>amyloid-beta</p></def></def-item><def-item><term>FXN</term><def><p>Frataxin.</p></def></def-item></def-list></glossary></back></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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