SIRT1 protects the heart from ER stress-induced cell death through eIF2α deacetylation.
Identifieur interne : 001161 ( PubMed/Corpus ); précédent : 001160; suivant : 001162SIRT1 protects the heart from ER stress-induced cell death through eIF2α deacetylation.
Auteurs : Alexandre Prola ; Julie Pires Da Silva ; Arnaud Guilbert ; Lola Lecru ; Jérôme Piquereau ; Maxance Ribeiro ; Philippe Mateo ; Mélanie Gressette ; Dominique Fortin ; Céline Boursier ; Cindy Gallerne ; Anaïs Caillard ; Jane-Lise Samuel ; Hélène François ; David A. Sinclair ; Pierre Eid ; Renée Ventura-Clapier ; Anne Garnier ; Christophe LemaireSource :
- Cell death and differentiation [ 1476-5403 ] ; 2017.
Abstract
Over the past decade, endoplasmic reticulum (ER) stress has emerged as an important mechanism involved in the pathogenesis of cardiovascular diseases including heart failure. Cardiac therapy based on ER stress modulation is viewed as a promising avenue toward effective therapies for the diseased heart. Here, we tested whether sirtuin-1 (SIRT1), a NAD(+)-dependent deacetylase, participates in modulating ER stress response in the heart. Using cardiomyocytes and adult-inducible SIRT1 knockout mice, we demonstrate that SIRT1 inhibition or deficiency increases ER stress-induced cardiac injury, whereas activation of SIRT1 by the SIRT1-activating compound STAC-3 is protective. Analysis of the expression of markers of the three main branches of the unfolded protein response (i.e., PERK/eIF2α, ATF6 and IRE1) showed that SIRT1 protects cardiomyocytes from ER stress-induced apoptosis by attenuating PERK/eIF2α pathway activation. We also present evidence that SIRT1 physically interacts with and deacetylates eIF2α. Mass spectrometry analysis identified lysines K141 and K143 as the acetylation sites on eIF2α targeted by SIRT1. Furthermore, mutation of K143 to arginine to mimic eIF2α deacetylation confers protection against ER stress-induced apoptosis. Collectively, our findings indicate that eIF2α deacetylation on lysine K143 by SIRT1 is a novel regulatory mechanism for protecting cardiac cells from ER stress and suggest that activation of SIRT1 has potential as a therapeutic approach to protect the heart against ER stress-induced injury.
DOI: 10.1038/cdd.2016.138
PubMed: 27911441
Links to Exploration step
pubmed:27911441Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">SIRT1 protects the heart from ER stress-induced cell death through eIF2α deacetylation.</title><author><name sortKey="Prola, Alexandre" sort="Prola, Alexandre" uniqKey="Prola A" first="Alexandre" last="Prola">Alexandre Prola</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Silva, Julie Pires Da" sort="Silva, Julie Pires Da" uniqKey="Silva J" first="Julie Pires Da" last="Silva">Julie Pires Da Silva</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Guilbert, Arnaud" sort="Guilbert, Arnaud" uniqKey="Guilbert A" first="Arnaud" last="Guilbert">Arnaud Guilbert</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Lecru, Lola" sort="Lecru, Lola" uniqKey="Lecru L" first="Lola" last="Lecru">Lola Lecru</name><affiliation><nlm:affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Piquereau, Jerome" sort="Piquereau, Jerome" uniqKey="Piquereau J" first="Jérôme" last="Piquereau">Jérôme Piquereau</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Ribeiro, Maxance" sort="Ribeiro, Maxance" uniqKey="Ribeiro M" first="Maxance" last="Ribeiro">Maxance Ribeiro</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Mateo, Philippe" sort="Mateo, Philippe" uniqKey="Mateo P" first="Philippe" last="Mateo">Philippe Mateo</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Gressette, Melanie" sort="Gressette, Melanie" uniqKey="Gressette M" first="Mélanie" last="Gressette">Mélanie Gressette</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Fortin, Dominique" sort="Fortin, Dominique" uniqKey="Fortin D" first="Dominique" last="Fortin">Dominique Fortin</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Boursier, Celine" sort="Boursier, Celine" uniqKey="Boursier C" first="Céline" last="Boursier">Céline Boursier</name><affiliation><nlm:affiliation>Institut Paris-Sud d'Innovation Thérapeutique, Univ Paris-Sud, Université Paris-Saclay, Chatenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Gallerne, Cindy" sort="Gallerne, Cindy" uniqKey="Gallerne C" first="Cindy" last="Gallerne">Cindy Gallerne</name><affiliation><nlm:affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Caillard, Anais" sort="Caillard, Anais" uniqKey="Caillard A" first="Anaïs" last="Caillard">Anaïs Caillard</name><affiliation><nlm:affiliation>UMR-S 942, INSERM, Univ Denis Diderot, Hôpital Lariboisière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Samuel, Jane Lise" sort="Samuel, Jane Lise" uniqKey="Samuel J" first="Jane-Lise" last="Samuel">Jane-Lise Samuel</name><affiliation><nlm:affiliation>UMR-S 942, INSERM, Univ Denis Diderot, Hôpital Lariboisière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Francois, Helene" sort="Francois, Helene" uniqKey="Francois H" first="Hélène" last="François">Hélène François</name><affiliation><nlm:affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Sinclair, David A" sort="Sinclair, David A" uniqKey="Sinclair D" first="David A" last="Sinclair">David A. Sinclair</name><affiliation><nlm:affiliation>Glenn Labs for the Biological Mechanisms of Aging, Department of Genetics, Harvard Medical School, Boston, MA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Eid, Pierre" sort="Eid, Pierre" uniqKey="Eid P" first="Pierre" last="Eid">Pierre Eid</name><affiliation><nlm:affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Ventura Clapier, Renee" sort="Ventura Clapier, Renee" uniqKey="Ventura Clapier R" first="Renée" last="Ventura-Clapier">Renée Ventura-Clapier</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Garnier, Anne" sort="Garnier, Anne" uniqKey="Garnier A" first="Anne" last="Garnier">Anne Garnier</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Lemaire, Christophe" sort="Lemaire, Christophe" uniqKey="Lemaire C" first="Christophe" last="Lemaire">Christophe Lemaire</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:27911441</idno><idno type="pmid">27911441</idno><idno type="doi">10.1038/cdd.2016.138</idno><idno type="wicri:Area/PubMed/Corpus">001161</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001161</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">SIRT1 protects the heart from ER stress-induced cell death through eIF2α deacetylation.</title><author><name sortKey="Prola, Alexandre" sort="Prola, Alexandre" uniqKey="Prola A" first="Alexandre" last="Prola">Alexandre Prola</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Silva, Julie Pires Da" sort="Silva, Julie Pires Da" uniqKey="Silva J" first="Julie Pires Da" last="Silva">Julie Pires Da Silva</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Guilbert, Arnaud" sort="Guilbert, Arnaud" uniqKey="Guilbert A" first="Arnaud" last="Guilbert">Arnaud Guilbert</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Lecru, Lola" sort="Lecru, Lola" uniqKey="Lecru L" first="Lola" last="Lecru">Lola Lecru</name><affiliation><nlm:affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Piquereau, Jerome" sort="Piquereau, Jerome" uniqKey="Piquereau J" first="Jérôme" last="Piquereau">Jérôme Piquereau</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Ribeiro, Maxance" sort="Ribeiro, Maxance" uniqKey="Ribeiro M" first="Maxance" last="Ribeiro">Maxance Ribeiro</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Mateo, Philippe" sort="Mateo, Philippe" uniqKey="Mateo P" first="Philippe" last="Mateo">Philippe Mateo</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Gressette, Melanie" sort="Gressette, Melanie" uniqKey="Gressette M" first="Mélanie" last="Gressette">Mélanie Gressette</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Fortin, Dominique" sort="Fortin, Dominique" uniqKey="Fortin D" first="Dominique" last="Fortin">Dominique Fortin</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Boursier, Celine" sort="Boursier, Celine" uniqKey="Boursier C" first="Céline" last="Boursier">Céline Boursier</name><affiliation><nlm:affiliation>Institut Paris-Sud d'Innovation Thérapeutique, Univ Paris-Sud, Université Paris-Saclay, Chatenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Gallerne, Cindy" sort="Gallerne, Cindy" uniqKey="Gallerne C" first="Cindy" last="Gallerne">Cindy Gallerne</name><affiliation><nlm:affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Caillard, Anais" sort="Caillard, Anais" uniqKey="Caillard A" first="Anaïs" last="Caillard">Anaïs Caillard</name><affiliation><nlm:affiliation>UMR-S 942, INSERM, Univ Denis Diderot, Hôpital Lariboisière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Samuel, Jane Lise" sort="Samuel, Jane Lise" uniqKey="Samuel J" first="Jane-Lise" last="Samuel">Jane-Lise Samuel</name><affiliation><nlm:affiliation>UMR-S 942, INSERM, Univ Denis Diderot, Hôpital Lariboisière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Francois, Helene" sort="Francois, Helene" uniqKey="Francois H" first="Hélène" last="François">Hélène François</name><affiliation><nlm:affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Sinclair, David A" sort="Sinclair, David A" uniqKey="Sinclair D" first="David A" last="Sinclair">David A. Sinclair</name><affiliation><nlm:affiliation>Glenn Labs for the Biological Mechanisms of Aging, Department of Genetics, Harvard Medical School, Boston, MA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Eid, Pierre" sort="Eid, Pierre" uniqKey="Eid P" first="Pierre" last="Eid">Pierre Eid</name><affiliation><nlm:affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Ventura Clapier, Renee" sort="Ventura Clapier, Renee" uniqKey="Ventura Clapier R" first="Renée" last="Ventura-Clapier">Renée Ventura-Clapier</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Garnier, Anne" sort="Garnier, Anne" uniqKey="Garnier A" first="Anne" last="Garnier">Anne Garnier</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author><author><name sortKey="Lemaire, Christophe" sort="Lemaire, Christophe" uniqKey="Lemaire C" first="Christophe" last="Lemaire">Christophe Lemaire</name><affiliation><nlm:affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Cell death and differentiation</title><idno type="eISSN">1476-5403</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Over the past decade, endoplasmic reticulum (ER) stress has emerged as an important mechanism involved in the pathogenesis of cardiovascular diseases including heart failure. Cardiac therapy based on ER stress modulation is viewed as a promising avenue toward effective therapies for the diseased heart. Here, we tested whether sirtuin-1 (SIRT1), a NAD(+)-dependent deacetylase, participates in modulating ER stress response in the heart. Using cardiomyocytes and adult-inducible SIRT1 knockout mice, we demonstrate that SIRT1 inhibition or deficiency increases ER stress-induced cardiac injury, whereas activation of SIRT1 by the SIRT1-activating compound STAC-3 is protective. Analysis of the expression of markers of the three main branches of the unfolded protein response (i.e., PERK/eIF2α, ATF6 and IRE1) showed that SIRT1 protects cardiomyocytes from ER stress-induced apoptosis by attenuating PERK/eIF2α pathway activation. We also present evidence that SIRT1 physically interacts with and deacetylates eIF2α. Mass spectrometry analysis identified lysines K141 and K143 as the acetylation sites on eIF2α targeted by SIRT1. Furthermore, mutation of K143 to arginine to mimic eIF2α deacetylation confers protection against ER stress-induced apoptosis. Collectively, our findings indicate that eIF2α deacetylation on lysine K143 by SIRT1 is a novel regulatory mechanism for protecting cardiac cells from ER stress and suggest that activation of SIRT1 has potential as a therapeutic approach to protect the heart against ER stress-induced injury.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">27911441</PMID><DateCreated><Year>2016</Year><Month>12</Month><Day>02</Day></DateCreated><DateRevised><Year>2017</Year><Month>04</Month><Day>03</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-5403</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>2</Issue><PubDate><Year>2017</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Cell death and differentiation</Title><ISOAbbreviation>Cell Death Differ.</ISOAbbreviation></Journal><ArticleTitle>SIRT1 protects the heart from ER stress-induced cell death through eIF2α deacetylation.</ArticleTitle><Pagination><MedlinePgn>343-356</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/cdd.2016.138</ELocationID><Abstract><AbstractText>Over the past decade, endoplasmic reticulum (ER) stress has emerged as an important mechanism involved in the pathogenesis of cardiovascular diseases including heart failure. Cardiac therapy based on ER stress modulation is viewed as a promising avenue toward effective therapies for the diseased heart. Here, we tested whether sirtuin-1 (SIRT1), a NAD(+)-dependent deacetylase, participates in modulating ER stress response in the heart. Using cardiomyocytes and adult-inducible SIRT1 knockout mice, we demonstrate that SIRT1 inhibition or deficiency increases ER stress-induced cardiac injury, whereas activation of SIRT1 by the SIRT1-activating compound STAC-3 is protective. Analysis of the expression of markers of the three main branches of the unfolded protein response (i.e., PERK/eIF2α, ATF6 and IRE1) showed that SIRT1 protects cardiomyocytes from ER stress-induced apoptosis by attenuating PERK/eIF2α pathway activation. We also present evidence that SIRT1 physically interacts with and deacetylates eIF2α. Mass spectrometry analysis identified lysines K141 and K143 as the acetylation sites on eIF2α targeted by SIRT1. Furthermore, mutation of K143 to arginine to mimic eIF2α deacetylation confers protection against ER stress-induced apoptosis. Collectively, our findings indicate that eIF2α deacetylation on lysine K143 by SIRT1 is a novel regulatory mechanism for protecting cardiac cells from ER stress and suggest that activation of SIRT1 has potential as a therapeutic approach to protect the heart against ER stress-induced injury.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Prola</LastName><ForeName>Alexandre</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Silva</LastName><ForeName>Julie Pires Da</ForeName><Initials>JP</Initials><AffiliationInfo><Affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guilbert</LastName><ForeName>Arnaud</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lecru</LastName><ForeName>Lola</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Piquereau</LastName><ForeName>Jérôme</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ribeiro</LastName><ForeName>Maxance</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mateo</LastName><ForeName>Philippe</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gressette</LastName><ForeName>Mélanie</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fortin</LastName><ForeName>Dominique</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boursier</LastName><ForeName>Céline</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Institut Paris-Sud d'Innovation Thérapeutique, Univ Paris-Sud, Université Paris-Saclay, Chatenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gallerne</LastName><ForeName>Cindy</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Caillard</LastName><ForeName>Anaïs</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>UMR-S 942, INSERM, Univ Denis Diderot, Hôpital Lariboisière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Samuel</LastName><ForeName>Jane-Lise</ForeName><Initials>JL</Initials><AffiliationInfo><Affiliation>UMR-S 942, INSERM, Univ Denis Diderot, Hôpital Lariboisière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>François</LastName><ForeName>Hélène</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sinclair</LastName><ForeName>David A</ForeName><Initials>DA</Initials><AffiliationInfo><Affiliation>Glenn Labs for the Biological Mechanisms of Aging, Department of Genetics, Harvard Medical School, Boston, MA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, New South Wales, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eid</LastName><ForeName>Pierre</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>UMR-S 1014, INSERM, Univ Paris-Sud, Université Paris-Saclay, Hôpital Paul Brousse, Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ventura-Clapier</LastName><ForeName>Renée</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Garnier</LastName><ForeName>Anne</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lemaire</LastName><ForeName>Christophe</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>UMR-S 1180, INSERM, Univ Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université Versailles St. Quentin, Université Paris-Saclay, Versailles, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AG028730</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 AG028730</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>12</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Cell Death Differ</MedlineTA><NlmUniqueID>9437445</NlmUniqueID><ISSNLinking>1350-9047</ISSNLinking></MedlineJournalInfo><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2009 Dec 22;4(12):e8414</RefSource><PMID Version="1">20027304</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Int J Cardiol. 2015 Jul 15;191:36-45</RefSource><PMID Version="1">25965594</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>EMBO J. 1999 Jan 4;18(1):96-108</RefSource><PMID Version="1">9878054</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Mol Cell Cardiol. 2010 Jun;48(6):1105-10</RefSource><PMID Version="1">19913545</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 2013 Mar 8;339(6124):1216-9</RefSource><PMID Version="1">23471411</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Gen Physiol Biophys. 2012 Jun;31(2):141-51</RefSource><PMID Version="1">22781817</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2005 Mar 3;434(7029):113-8</RefSource><PMID Version="1">15744310</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Mol Pathol. 2012 Feb;92(1):97-104</RefSource><PMID Version="1">22101259</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Annu Rev Pathol. 2015;10:173-94</RefSource><PMID Version="1">25387057</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2006 May 12;98 (9):1186-93</RefSource><PMID Version="1">16601230</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cardiovasc Res. 2011 May 1;90(2):276-84</RefSource><PMID Version="1">21115502</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Cell Biochem. 2012 May;364(1-2):59-70</RefSource><PMID Version="1">22270541</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Dev Cell. 2007 Sep;13(3):365-76</RefSource><PMID Version="1">17765680</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Anal Chem. 1996 Mar 1;68(5):850-8</RefSource><PMID Version="1">8779443</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Cell. 2000 Nov;6(5):1099-108</RefSource><PMID Version="1">11106749</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur Heart J. 2015 Dec 21;36(48):3404-12</RefSource><PMID Version="1">26112889</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell. 2013 Jul 18;154(2):430-41</RefSource><PMID Version="1">23870130</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Cell. 2011 Dec 23;44(6):851-63</RefSource><PMID Version="1">22195961</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Cell Biol. 2011 Mar;13(3):184-90</RefSource><PMID Version="1">21364565</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell Mol Life Sci. 2013 Oct;70(19):3493-511</RefSource><PMID Version="1">23354059</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circulation. 2010 Jul 27;122(4):361-9</RefSource><PMID Version="1">20625112</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Free Radic Biol Med. 2015 Nov;88(Pt B):233-42</RefSource><PMID Version="1">26051167</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Annu Rev Pathol. 2010;5:253-95</RefSource><PMID Version="1">20078221</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Rev Mol Cell Biol. 2012 Jan 18;13(2):89-102</RefSource><PMID Version="1">22251901</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Mol Cell Cardiol. 2011 Jan;50(1):107-16</RefSource><PMID Version="1">21035453</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2011 Mar 15;108(11):4316-21</RefSource><PMID Version="1">21368187</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Commun. 2015 May 26;6:7215</RefSource><PMID Version="1">26008601</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Rev Mol Cell Biol. 2007 Jul;8(7):519-29</RefSource><PMID Version="1">17565364</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem Biophys Res Commun. 2006 Jul 14;345(4):1600-5</RefSource><PMID Version="1">16735028</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2015 Jul;1852(7):1311-22</RefSource><PMID Version="1">25766107</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Antioxid Redox Signal. 2011 Nov 1;15(9):2407-24</RefSource><PMID Version="1">21542787</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circulation. 2010 Nov 23;122(21):2170-82</RefSource><PMID Version="1">21060073</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Rev Drug Discov. 2013 Sep;12(9):703-19</RefSource><PMID Version="1">23989796</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell. 2007 Jun 29;129(7):1337-49</RefSource><PMID Version="1">17604722</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2006 Aug 4;99(3):275-82</RefSource><PMID Version="1">16794188</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trends Genet. 2014 Jul;30(7):271-86</RefSource><PMID Version="1">24877878</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochem J. 2011 Jan 1;433(1):245-52</RefSource><PMID Version="1">20955178</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2016 Sep 16;119(7):865-79</RefSource><PMID Version="1">27461939</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2012;7(2):e31431</RefSource><PMID Version="1">22363646</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Sci Rep. 2011;1:150</RefSource><PMID Version="1">22355666</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Circ Res. 2007 May 25;100(10 ):1512-21</RefSource><PMID Version="1">17446436</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proteomics. 2013 Sep;13(17):2552-62</RefSource><PMID Version="1">23836775</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Comp Med. 2009 Aug;59(4):339-43</RefSource><PMID Version="1">19712573</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Am Coll Cardiol. 2007 Sep 11;50(11):1029-37</RefSource><PMID Version="1">17825711</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Br J Pharmacol. 1999 May;127(1):65-74</RefSource><PMID Version="1">10369457</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Heart Circ Physiol. 2015 Aug 1;309(3):H459-70</RefSource><PMID Version="1">26055788</PMID></CommentsCorrections></CommentsCorrectionsList><CoiStatement>DAS consults for GlaxoSmithKline, Metrobiotech, Ovascience and BigDataBio. The remaining authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>01</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>09</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>10</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="pmc-release"><Year>2018</Year><Month>02</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>12</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>12</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>12</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27911441</ArticleId><ArticleId IdType="pii">cdd2016138</ArticleId><ArticleId IdType="doi">10.1038/cdd.2016.138</ArticleId><ArticleId IdType="pmc">PMC5299716</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Asie/explor/AustralieFrV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001161 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 001161 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Asie
|area= AustralieFrV1
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:27911441
|texte= SIRT1 protects the heart from ER stress-induced cell death through eIF2α deacetylation.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:27911441" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a AustralieFrV1
| This area was generated with Dilib version V0.6.33. |  |