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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Monoamine oxidases as sources of oxidants in the
heart</title><author><name sortKey="Kaludercic, Nina" sort="Kaludercic, Nina" uniqKey="Kaludercic N" first="Nina" last="Kaludercic">Nina Kaludercic</name><affiliation><nlm:aff id="A1">Neuroscience Institute, National Research Council of Italy (CNR), Padua, Italy</nlm:aff></affiliation></author><author><name sortKey="Mialet Perez, Jeanne" sort="Mialet Perez, Jeanne" uniqKey="Mialet Perez J" first="Jeanne" last="Mialet-Perez">Jeanne Mialet-Perez</name><affiliation><nlm:aff id="A2">INSERM UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Paul Sabatier University, Toulouse, France</nlm:aff></affiliation></author><author><name sortKey="Paolocci, Nazareno" sort="Paolocci, Nazareno" uniqKey="Paolocci N" first="Nazareno" last="Paolocci">Nazareno Paolocci</name><affiliation><nlm:aff id="A4">Johns Hopkins Medical Institutions, Baltimore, MD, USA</nlm:aff></affiliation></author><author><name sortKey="Parini, Angelo" sort="Parini, Angelo" uniqKey="Parini A" first="Angelo" last="Parini">Angelo Parini</name><affiliation><nlm:aff id="A2">INSERM UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Paul Sabatier University, Toulouse, France</nlm:aff></affiliation></author><author><name sortKey="Di Lisa, Fabio" sort="Di Lisa, Fabio" uniqKey="Di Lisa F" first="Fabio" last="Di Lisa">Fabio Di Lisa</name><affiliation><nlm:aff id="A1">Neuroscience Institute, National Research Council of Italy (CNR), Padua, Italy</nlm:aff></affiliation><affiliation><nlm:aff id="A5">Department of Biomedical Sciences, University of Padua, Italy</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24412580</idno><idno type="pmc">4048760</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4048760</idno><idno type="RBID">PMC:4048760</idno><idno type="doi">10.1016/j.yjmcc.2013.12.032</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000576</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000576</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Monoamine oxidases as sources of oxidants in the
heart</title><author><name sortKey="Kaludercic, Nina" sort="Kaludercic, Nina" uniqKey="Kaludercic N" first="Nina" last="Kaludercic">Nina Kaludercic</name><affiliation><nlm:aff id="A1">Neuroscience Institute, National Research Council of Italy (CNR), Padua, Italy</nlm:aff></affiliation></author><author><name sortKey="Mialet Perez, Jeanne" sort="Mialet Perez, Jeanne" uniqKey="Mialet Perez J" first="Jeanne" last="Mialet-Perez">Jeanne Mialet-Perez</name><affiliation><nlm:aff id="A2">INSERM UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Paul Sabatier University, Toulouse, France</nlm:aff></affiliation></author><author><name sortKey="Paolocci, Nazareno" sort="Paolocci, Nazareno" uniqKey="Paolocci N" first="Nazareno" last="Paolocci">Nazareno Paolocci</name><affiliation><nlm:aff id="A4">Johns Hopkins Medical Institutions, Baltimore, MD, USA</nlm:aff></affiliation></author><author><name sortKey="Parini, Angelo" sort="Parini, Angelo" uniqKey="Parini A" first="Angelo" last="Parini">Angelo Parini</name><affiliation><nlm:aff id="A2">INSERM UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Paul Sabatier University, Toulouse, France</nlm:aff></affiliation></author><author><name sortKey="Di Lisa, Fabio" sort="Di Lisa, Fabio" uniqKey="Di Lisa F" first="Fabio" last="Di Lisa">Fabio Di Lisa</name><affiliation><nlm:aff id="A1">Neuroscience Institute, National Research Council of Italy (CNR), Padua, Italy</nlm:aff></affiliation><affiliation><nlm:aff id="A5">Department of Biomedical Sciences, University of Padua, Italy</nlm:aff></affiliation></author></analytic><series><title level="j">Journal of molecular and cellular cardiology</title><idno type="ISSN">0022-2828</idno><idno type="eISSN">1095-8584</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 id="P2">Oxidative stress can be generated at several sites within the
mitochondria. Among these, monoamine oxidases (MAO) have been described as a
prominent source. MAO are mitochondrial flavoenzymes responsible for the
oxidative deamination of catecholamines, serotonin and biogenic amines, and
during this process they generate H<sub>2</sub>O<sub>2</sub> and aldehyde
intermediates. The role of MAO in cardiovascular pathophysiology has only
recently gathered some attention since it has been demonstrated that both
H<sub>2</sub>O<sub>2</sub> and aldehydes may target mitochondrial function
and consequently affect function and viability of the myocardium. In the present
review, we will discuss the role of MAO in catecholamine and serotonin clearance
and cycling in relation to cardiac structure and function. The relevant
contribution of each MAO isoform (MAO-A or -B) will be discussed in relation to
mitochondrial dysfunction and myocardial injury. Finally, we will examine both
beneficial effects of their pharmacological or genetic inhibition along with
potential adverse effects observed at baseline in MAO knockout mice, as well as
the deleterious effects following their over-expression specifically at
cardiomyocyte level.</p></div></front></TEI><pmc article-type="research-article"><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">0262322</journal-id><journal-id journal-id-type="pubmed-jr-id">4968</journal-id><journal-id journal-id-type="nlm-ta">J Mol Cell Cardiol</journal-id><journal-id journal-id-type="iso-abbrev">J. Mol. Cell. Cardiol.</journal-id><journal-title-group><journal-title>Journal of molecular and cellular cardiology</journal-title></journal-title-group><issn pub-type="ppub">0022-2828</issn><issn pub-type="epub">1095-8584</issn></journal-meta><article-meta><article-id pub-id-type="pmid">24412580</article-id><article-id pub-id-type="pmc">4048760</article-id><article-id pub-id-type="doi">10.1016/j.yjmcc.2013.12.032</article-id><article-id pub-id-type="manuscript">NIHMS554707</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Monoamine oxidases as sources of oxidants in the
heart</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Kaludercic</surname><given-names>Nina</given-names></name><xref ref-type="aff" rid="A1">a</xref></contrib><contrib contrib-type="author"><name><surname>Mialet-Perez</surname><given-names>Jeanne</given-names></name><xref ref-type="aff" rid="A2">b</xref><xref ref-type="aff" rid="A3">c</xref></contrib><contrib contrib-type="author"><name><surname>Paolocci</surname><given-names>Nazareno</given-names></name><xref ref-type="aff" rid="A4">d</xref></contrib><contrib contrib-type="author"><name><surname>Parini</surname><given-names>Angelo</given-names></name><xref ref-type="aff" rid="A2">b</xref><xref ref-type="aff" rid="A3">c</xref></contrib><contrib contrib-type="author"><name><surname>Di Lisa</surname><given-names>Fabio</given-names></name><xref ref-type="aff" rid="A1">a</xref><xref ref-type="aff" rid="A5">e</xref><xref rid="FN1" ref-type="author-notes">*</xref></contrib></contrib-group><aff id="A1"><label>a</label>Neuroscience Institute, National Research Council of Italy (CNR), Padua, Italy</aff><aff id="A2"><label>b</label>INSERM UMR 1048, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France</aff><aff id="A3"><label>c</label>Paul Sabatier University, Toulouse, France</aff><aff id="A4"><label>d</label>Johns Hopkins Medical Institutions, Baltimore, MD, USA</aff><aff id="A5"><label>e</label>Department of Biomedical Sciences, University of Padua, Italy</aff><author-notes><corresp id="FN1"><label>*</label>Corresponding Author: Prof. Fabio Di Lisa, Department of
Biomedical Sciences, University of Padua, Viale G. Colombo 3, 35131 Padua,
Italy, Tel: +39 0498276132, Fax: +39 0498276040,
<email>dilisa@bio.unipd.it</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>21</day><month>2</month><year>2014</year></pub-date><pub-date pub-type="epub"><day>9</day><month>1</month><year>2014</year></pub-date><pub-date pub-type="ppub"><month>8</month><year>2014</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>8</month><year>2015</year></pub-date><volume>0</volume><fpage>34</fpage><lpage>42</lpage><pmc-comment>elocation-id from pubmed: 10.1016/j.yjmcc.2013.12.032</pmc-comment>
<permissions><copyright-statement>© 2013 Elsevier Ltd. All rights
reserved.</copyright-statement><copyright-year>2013</copyright-year></permissions><abstract><p id="P2">Oxidative stress can be generated at several sites within the
mitochondria. Among these, monoamine oxidases (MAO) have been described as a
prominent source. MAO are mitochondrial flavoenzymes responsible for the
oxidative deamination of catecholamines, serotonin and biogenic amines, and
during this process they generate H<sub>2</sub>O<sub>2</sub> and aldehyde
intermediates. The role of MAO in cardiovascular pathophysiology has only
recently gathered some attention since it has been demonstrated that both
H<sub>2</sub>O<sub>2</sub> and aldehydes may target mitochondrial function
and consequently affect function and viability of the myocardium. In the present
review, we will discuss the role of MAO in catecholamine and serotonin clearance
and cycling in relation to cardiac structure and function. The relevant
contribution of each MAO isoform (MAO-A or -B) will be discussed in relation to
mitochondrial dysfunction and myocardial injury. Finally, we will examine both
beneficial effects of their pharmacological or genetic inhibition along with
potential adverse effects observed at baseline in MAO knockout mice, as well as
the deleterious effects following their over-expression specifically at
cardiomyocyte level.</p></abstract><kwd-group><kwd>monoamine oxidase</kwd><kwd>oxidative stress</kwd><kwd>mitochondrial dysfunction</kwd><kwd>heart failure</kwd><kwd>ischemia/reperfusion injury</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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