Autophagy modulation as a potential therapeutic target for diverse diseases
Identifieur interne : 000449 ( Istex/Curation ); précédent : 000448; suivant : 000450Autophagy modulation as a potential therapeutic target for diverse diseases
Auteurs : David C. Rubinsztein [Royaume-Uni] ; Patrice Codogno [France] ; Beth Levine [États-Unis]Source :
- Nature Reviews Drug Discovery [ 1474-1776 ] ; 2012-09.
Abstract
Autophagy is an essential, conserved lysosomal degradation pathway that controls the quality of the cytoplasm by eliminating protein aggregates and damaged organelles. It begins when double-membraned autophagosomes engulf portions of the cytoplasm, which is followed by fusion of these vesicles with lysosomes and degradation of the autophagic contents. In addition to its vital homeostatic role, this degradation pathway is involved in various human disorders, including metabolic conditions, neurodegenerative diseases, cancers and infectious diseases. This article provides an overview of the mechanisms and regulation of autophagy, the role of this pathway in disease and strategies for therapeutic modulation.
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DOI: 10.1038/nrd3802
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Rubinsztein</name><affiliation wicri:level="1"><mods:affiliation>Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Wellcome Trust/MRC Building, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY, UK.</mods:affiliation><country xml:lang="fr" wicri:curation="lc">Royaume-Uni</country><wicri:regionArea>Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Wellcome Trust/MRC Building, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY</wicri:regionArea></affiliation><affiliation><mods:affiliation>All authors contributed equally to this work.</mods:affiliation><wicri:noCountry code="no comma">All authors contributed equally to this work.</wicri:noCountry></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: dcr1000@cam.ac.uk</mods:affiliation><country wicri:rule="url">Royaume-Uni</country></affiliation></author><author><name sortKey="Codogno, Patrice" sort="Codogno, Patrice" uniqKey="Codogno P" first="Patrice" last="Codogno">Patrice Codogno</name><affiliation wicri:level="1"><mods:affiliation>Faculté de Pharmacie, Institut National de la Santé et de la Recherche Médicale (INSERM) UMR984, Université Paris-Sud 11, 5 rue Jean-Baptiste Clément, 92296 Châtenay-Malabry, France.</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Faculté de Pharmacie, Institut National de la Santé et de la Recherche Médicale (INSERM) UMR984, Université Paris-Sud 11, 5 rue Jean-Baptiste Clément, 92296 Châtenay-Malabry</wicri:regionArea></affiliation><affiliation><mods:affiliation>All authors contributed equally to this work.</mods:affiliation><wicri:noCountry code="no comma">All authors contributed equally to this work.</wicri:noCountry></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: patrice.codogno@u-psud.fr</mods:affiliation><country wicri:rule="url">France</country></affiliation></author><author><name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name><affiliation wicri:level="1"><mods:affiliation>Departments of Internal Medicine and Microbiology, Center for Autophagy Research, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.</mods:affiliation><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Departments of Internal Medicine and Microbiology, Center for Autophagy Research, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390</wicri:regionArea></affiliation><affiliation><mods:affiliation>All authors contributed equally to this work.</mods:affiliation><wicri:noCountry code="no comma">All authors contributed equally to this work.</wicri:noCountry></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: beth.levine@utsouthwestern.edu</mods:affiliation><country wicri:rule="url">États-Unis</country></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:32FD5CD49AA6E68C452BCC94E3DF157227A9BC54</idno><date when="2012" year="2012">2012</date><idno type="doi">10.1038/nrd3802</idno><idno type="url">https://api.istex.fr/ark:/67375/GT4-26JJ9W0B-4/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000449</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000449</idno><idno type="wicri:Area/Istex/Curation">000449</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Autophagy modulation as a potential therapeutic target for diverse diseases</title><author><name sortKey="Rubinsztein, David C" sort="Rubinsztein, David C" uniqKey="Rubinsztein D" first="David C." last="Rubinsztein">David C. Rubinsztein</name><affiliation wicri:level="1"><mods:affiliation>Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Wellcome Trust/MRC Building, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY, UK.</mods:affiliation><country xml:lang="fr" wicri:curation="lc">Royaume-Uni</country><wicri:regionArea>Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Wellcome Trust/MRC Building, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY</wicri:regionArea></affiliation><affiliation><mods:affiliation>All authors contributed equally to this work.</mods:affiliation></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: dcr1000@cam.ac.uk</mods:affiliation><country wicri:rule="url">Royaume-Uni</country></affiliation></author><author><name sortKey="Codogno, Patrice" sort="Codogno, Patrice" uniqKey="Codogno P" first="Patrice" last="Codogno">Patrice Codogno</name><affiliation wicri:level="1"><mods:affiliation>Faculté de Pharmacie, Institut National de la Santé et de la Recherche Médicale (INSERM) UMR984, Université Paris-Sud 11, 5 rue Jean-Baptiste Clément, 92296 Châtenay-Malabry, France.</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Faculté de Pharmacie, Institut National de la Santé et de la Recherche Médicale (INSERM) UMR984, Université Paris-Sud 11, 5 rue Jean-Baptiste Clément, 92296 Châtenay-Malabry</wicri:regionArea></affiliation><affiliation><mods:affiliation>All authors contributed equally to this work.</mods:affiliation></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: patrice.codogno@u-psud.fr</mods:affiliation><country wicri:rule="url">France</country></affiliation></author><author><name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name><affiliation wicri:level="1"><mods:affiliation>Departments of Internal Medicine and Microbiology, Center for Autophagy Research, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.</mods:affiliation><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Departments of Internal Medicine and Microbiology, Center for Autophagy Research, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390</wicri:regionArea></affiliation><affiliation><mods:affiliation>All authors contributed equally to this work.</mods:affiliation></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: beth.levine@utsouthwestern.edu</mods:affiliation><country wicri:rule="url">États-Unis</country></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Nature Reviews Drug Discovery</title><idno type="ISSN">1474-1776</idno><idno type="eISSN">1474-1784</idno><imprint><publisher>Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.</publisher><date when="2012-09">2012-09</date><biblScope unit="vol">11</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="709">709</biblScope><biblScope unit="page" to="730">730</biblScope><date type="Copyright" when="2012">2012</date></imprint><idno type="ISSN">1474-1776</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1474-1776</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="eng">Autophagy is an essential, conserved lysosomal degradation pathway that controls the quality of the cytoplasm by eliminating protein aggregates and damaged organelles. It begins when double-membraned autophagosomes engulf portions of the cytoplasm, which is followed by fusion of these vesicles with lysosomes and degradation of the autophagic contents. In addition to its vital homeostatic role, this degradation pathway is involved in various human disorders, including metabolic conditions, neurodegenerative diseases, cancers and infectious diseases. This article provides an overview of the mechanisms and regulation of autophagy, the role of this pathway in disease and strategies for therapeutic modulation.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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