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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mitochondria and the autophagy-inflammation-cell death axis in organismal aging</title><author><name sortKey="Green, Douglas R" sort="Green, Douglas R" uniqKey="Green D" first="Douglas R." last="Green">Douglas R. Green</name><affiliation><nlm:aff id="A1">Department of Immunology, St Jude Children’s Research Hospital, Memphis, TN 38105, USA</nlm:aff></affiliation></author><author><name sortKey="Galluzzi, Lorenzo" sort="Galluzzi, Lorenzo" uniqKey="Galluzzi L" first="Lorenzo" last="Galluzzi">Lorenzo Galluzzi</name><affiliation><nlm:aff id="A2">INSERM, U848, F-94805 Villejuif, France</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Institut Gustave Roussy, F94805 Villejuif, France</nlm:aff></affiliation><affiliation><nlm:aff id="A4">Université Paris-Sud, Paris 11, F-94805 Villejuif, France</nlm:aff></affiliation></author><author><name sortKey="Kroemer, Guido" sort="Kroemer, Guido" uniqKey="Kroemer G" first="Guido" last="Kroemer">Guido Kroemer</name><affiliation><nlm:aff id="A2">INSERM, U848, F-94805 Villejuif, France</nlm:aff></affiliation><affiliation><nlm:aff id="A5">Metabolomics Platform, Institut Gustave Roussy, F-94805 Villejuif, France</nlm:aff></affiliation><affiliation><nlm:aff id="A6">Centre de Recherche des Cordeliers, F-75005 Paris, France</nlm:aff></affiliation><affiliation><nlm:aff id="A7">Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, F-75908 Paris, France</nlm:aff></affiliation><affiliation><nlm:aff id="A8">Université Paris Descartes, Paris 5, F-75270 Paris, France</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">21868666</idno><idno type="pmc">3405151</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3405151</idno><idno type="RBID">PMC:3405151</idno><idno type="doi">10.1126/science.1201940</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">000583</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000583</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Mitochondria and the autophagy-inflammation-cell death axis in organismal aging</title><author><name sortKey="Green, Douglas R" sort="Green, Douglas R" uniqKey="Green D" first="Douglas R." last="Green">Douglas R. Green</name><affiliation><nlm:aff id="A1">Department of Immunology, St Jude Children’s Research Hospital, Memphis, TN 38105, USA</nlm:aff></affiliation></author><author><name sortKey="Galluzzi, Lorenzo" sort="Galluzzi, Lorenzo" uniqKey="Galluzzi L" first="Lorenzo" last="Galluzzi">Lorenzo Galluzzi</name><affiliation><nlm:aff id="A2">INSERM, U848, F-94805 Villejuif, France</nlm:aff></affiliation><affiliation><nlm:aff id="A3">Institut Gustave Roussy, F94805 Villejuif, France</nlm:aff></affiliation><affiliation><nlm:aff id="A4">Université Paris-Sud, Paris 11, F-94805 Villejuif, France</nlm:aff></affiliation></author><author><name sortKey="Kroemer, Guido" sort="Kroemer, Guido" uniqKey="Kroemer G" first="Guido" last="Kroemer">Guido Kroemer</name><affiliation><nlm:aff id="A2">INSERM, U848, F-94805 Villejuif, France</nlm:aff></affiliation><affiliation><nlm:aff id="A5">Metabolomics Platform, Institut Gustave Roussy, F-94805 Villejuif, France</nlm:aff></affiliation><affiliation><nlm:aff id="A6">Centre de Recherche des Cordeliers, F-75005 Paris, France</nlm:aff></affiliation><affiliation><nlm:aff id="A7">Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, F-75908 Paris, France</nlm:aff></affiliation><affiliation><nlm:aff id="A8">Université Paris Descartes, Paris 5, F-75270 Paris, France</nlm:aff></affiliation></author></analytic><series><title level="j">Science (New York, N.y.)</title><idno type="ISSN">0036-8075</idno><idno type="eISSN">1095-9203</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>Summary</title><p id="P2">Alterations of mitochondrial functions are linked to multiple degenerative or acute diseases. As mitochondria age in our cells, they become progressively inefficient and potentially toxic, and acute damage can trigger the permeabilization of mitochondrial membranes to initiate apoptosis or necrosis. Moreover, mitochondria have an important role in pro-inflammatory signaling. Autophagic turnover of cellular constituents, be it general or specific for mitochondria (mitophagy), eliminates dysfunctional or damaged mitochondria, thus counteracting degeneration, dampening inflammation, and preventing unwarranted cell loss. Decreased expression of genes that regulate autophagy or mitophagy can cause degenerative diseases in which deficient quality control results in inflammation and the death of cell populations. Thus, a combination of mitochondrial dysfunction and insufficient autophagy may contribute to multiple aging-associated pathologies.</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">0404511</journal-id><journal-id journal-id-type="pubmed-jr-id">7473</journal-id><journal-id journal-id-type="nlm-ta">Science</journal-id><journal-id journal-id-type="iso-abbrev">Science</journal-id><journal-title-group><journal-title>Science (New York, N.y.)</journal-title></journal-title-group><issn pub-type="ppub">0036-8075</issn><issn pub-type="epub">1095-9203</issn></journal-meta><article-meta><article-id pub-id-type="pmid">21868666</article-id><article-id pub-id-type="pmc">3405151</article-id><article-id pub-id-type="doi">10.1126/science.1201940</article-id><article-id pub-id-type="manuscript">NIHMS392891</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Mitochondria and the autophagy-inflammation-cell death axis in organismal aging</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Green</surname><given-names>Douglas R.</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref rid="FN1" ref-type="author-notes">*</xref></contrib><contrib contrib-type="author"><name><surname>Galluzzi</surname><given-names>Lorenzo</given-names></name><xref ref-type="aff" rid="A2">2</xref><xref ref-type="aff" rid="A3">3</xref><xref ref-type="aff" rid="A4">4</xref></contrib><contrib contrib-type="author"><name><surname>Kroemer</surname><given-names>Guido</given-names></name><xref ref-type="aff" rid="A2">2</xref><xref ref-type="aff" rid="A5">5</xref><xref ref-type="aff" rid="A6">6</xref><xref ref-type="aff" rid="A7">7</xref><xref ref-type="aff" rid="A8">8</xref><xref rid="FN1" ref-type="author-notes">*</xref></contrib></contrib-group><aff id="A1"><label>1</label>Department of Immunology, St Jude Children’s Research Hospital, Memphis, TN 38105, USA</aff><aff id="A2"><label>2</label>INSERM, U848, F-94805 Villejuif, France</aff><aff id="A3"><label>3</label>Institut Gustave Roussy, F94805 Villejuif, France</aff><aff id="A4"><label>4</label>Université Paris-Sud, Paris 11, F-94805 Villejuif, France</aff><aff id="A5"><label>5</label>Metabolomics Platform, Institut Gustave Roussy, F-94805 Villejuif, France</aff><aff id="A6"><label>6</label>Centre de Recherche des Cordeliers, F-75005 Paris, France</aff><aff id="A7"><label>7</label>Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, F-75908 Paris, France</aff><aff id="A8"><label>8</label>Université Paris Descartes, Paris 5, F-75270 Paris, France</aff><author-notes><corresp id="FN1"><label>*</label>To whom correspondence should be addressed: <email>douglas.green@stjude.org</email> or <email>kroemer@orange.fr</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>11</day><month>7</month><year>2012</year></pub-date><pub-date pub-type="ppub"><day>26</day><month>8</month><year>2011</year></pub-date><pub-date pub-type="pmc-release"><day>25</day><month>7</month><year>2012</year></pub-date><volume>333</volume><issue>6046</issue><fpage>1109</fpage><lpage>1112</lpage><abstract><title>Summary</title><p id="P2">Alterations of mitochondrial functions are linked to multiple degenerative or acute diseases. As mitochondria age in our cells, they become progressively inefficient and potentially toxic, and acute damage can trigger the permeabilization of mitochondrial membranes to initiate apoptosis or necrosis. Moreover, mitochondria have an important role in pro-inflammatory signaling. Autophagic turnover of cellular constituents, be it general or specific for mitochondria (mitophagy), eliminates dysfunctional or damaged mitochondria, thus counteracting degeneration, dampening inflammation, and preventing unwarranted cell loss. Decreased expression of genes that regulate autophagy or mitophagy can cause degenerative diseases in which deficient quality control results in inflammation and the death of cell populations. Thus, a combination of mitochondrial dysfunction and insufficient autophagy may contribute to multiple aging-associated pathologies.</p></abstract><funding-group><award-group><funding-source country="United States">National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID</funding-source><award-id>R01 AI047891 || AI</award-id></award-group><award-group><funding-source country="United States">National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID</funding-source><award-id>R01 AI040646 || AI</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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