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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mitochondrial Turnover in the Heart</title><author><name sortKey="Gottlieb, Roberta A" sort="Gottlieb, Roberta A" uniqKey="Gottlieb R" first="Roberta A." last="Gottlieb">Roberta A. Gottlieb</name><affiliation><nlm:aff id="A1">BioScience Center, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182-4650, Phone: (619) 594-8981, Fax: (619) 594-8984</nlm:aff></affiliation></author><author><name sortKey="Gustafsson, Sa B" sort="Gustafsson, Sa B" uniqKey="Gustafsson " first=" Sa B." last="Gustafsson"> Sa B. Gustafsson</name><affiliation><nlm:aff id="A2">Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, 9500 Gilman Drive #0758 La Jolla, CA 92093-0758, Phone: (858) 822-5569, Fax: (858) 822-7558</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">21147177</idno><idno type="pmc">3335292</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3335292</idno><idno type="RBID">PMC:3335292</idno><idno type="doi">10.1016/j.bbamcr.2010.11.017</idno><date when="2010">2010</date><idno type="wicri:Area/Pmc/Corpus">000198</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000198</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Mitochondrial Turnover in the Heart</title><author><name sortKey="Gottlieb, Roberta A" sort="Gottlieb, Roberta A" uniqKey="Gottlieb R" first="Roberta A." last="Gottlieb">Roberta A. Gottlieb</name><affiliation><nlm:aff id="A1">BioScience Center, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182-4650, Phone: (619) 594-8981, Fax: (619) 594-8984</nlm:aff></affiliation></author><author><name sortKey="Gustafsson, Sa B" sort="Gustafsson, Sa B" uniqKey="Gustafsson " first=" Sa B." last="Gustafsson"> Sa B. Gustafsson</name><affiliation><nlm:aff id="A2">Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, 9500 Gilman Drive #0758 La Jolla, CA 92093-0758, Phone: (858) 822-5569, Fax: (858) 822-7558</nlm:aff></affiliation></author></analytic><series><title level="j">Biochimica et Biophysica Acta</title><idno type="ISSN">0006-3002</idno><idno type="eISSN">0006-3002</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P2">Mitochondrial quality control is increasingly recognized as an essential element in maintaining optimally functioning tissues. Mitochondrial quality control depends upon a balance between biogenesis and autophagic destruction. Mitochondrial dynamics (fusion and fission) allows for the redistribution of mitochondrial components. We speculate that this permits sorting of highly functional components into one end of a mitochondrion, while damaged components are segregated at the other end, to be jettisoned by asymmetric fission followed by selective mitophagy. Ischemic preconditioning requires autophagy/mitophagy, resulting in selective elimination of damaged mitochondria, leaving behind a population of robust mitochondria with a higher threshold for opening of the mitochondrial permeability transition pore. In this review we will consider the factors that regulate mitochondrial biogenesis and destruction, the machinery involved in both processes, and the biomedical consequences associated with altered mitochondrial turnover.</p></div></front></TEI><pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">0217513</journal-id><journal-id journal-id-type="pubmed-jr-id">1037</journal-id><journal-id journal-id-type="nlm-ta">Biochim Biophys Acta</journal-id><journal-title>Biochimica et Biophysica Acta</journal-title><issn pub-type="ppub">0006-3002</issn><issn pub-type="epub">0006-3002</issn></journal-meta><article-meta><article-id pub-id-type="pmid">21147177</article-id><article-id pub-id-type="pmc">3335292</article-id><article-id pub-id-type="doi">10.1016/j.bbamcr.2010.11.017</article-id><article-id pub-id-type="manuscript">NIHMS258631</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Mitochondrial Turnover in the Heart</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Gottlieb</surname><given-names>Roberta A.</given-names></name><degrees>M.D.</degrees><role>Director</role><xref rid="A1" ref-type="aff">1</xref><email>robbieg@sciences.sdsu.edu</email></contrib><contrib contrib-type="author"><name><surname>Gustafsson</surname><given-names>Åsa B.</given-names></name><degrees>Ph.D.</degrees><role>Assistant Professor</role><xref rid="A2" ref-type="aff">2</xref><email>abgustafsson@ucsd.edu</email></contrib></contrib-group><aff id="A1"><label>1</label>BioScience Center, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182-4650, Phone: (619) 594-8981, Fax: (619) 594-8984</aff><aff id="A2"><label>2</label>Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, 9500 Gilman Drive #0758 La Jolla, CA 92093-0758, Phone: (858) 822-5569, Fax: (858) 822-7558</aff><pub-date pub-type="nihms-submitted"><day>15</day><month>12</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>13</day><month>12</month><year>2010</year></pub-date><pub-date pub-type="ppub"><month>7</month><year>2011</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>7</month><year>2012</year></pub-date><volume>1813</volume><issue>7</issue><fpage>1295</fpage><lpage>1301</lpage><abstract><p id="P2">Mitochondrial quality control is increasingly recognized as an essential element in maintaining optimally functioning tissues. Mitochondrial quality control depends upon a balance between biogenesis and autophagic destruction. Mitochondrial dynamics (fusion and fission) allows for the redistribution of mitochondrial components. We speculate that this permits sorting of highly functional components into one end of a mitochondrion, while damaged components are segregated at the other end, to be jettisoned by asymmetric fission followed by selective mitophagy. Ischemic preconditioning requires autophagy/mitophagy, resulting in selective elimination of damaged mitochondria, leaving behind a population of robust mitochondria with a higher threshold for opening of the mitochondrial permeability transition pore. In this review we will consider the factors that regulate mitochondrial biogenesis and destruction, the machinery involved in both processes, and the biomedical consequences associated with altered mitochondrial turnover.</p></abstract><kwd-group><kwd>mitochondria</kwd><kwd>mitophagy</kwd><kwd>autophagy</kwd><kwd>mitochondrial turnover</kwd><kwd>cardioprotection</kwd></kwd-group><contract-num rid="HL1">R01 HL060590-12
||HL</contract-num><contract-num rid="AG1">R01 AG033283-04
||AG</contract-num><contract-sponsor id="HL1">National Heart, Lung, and Blood Institute : NHLBI</contract-sponsor><contract-sponsor id="AG1">National Institute on Aging : NIA</contract-sponsor></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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