Role of glutaredoxin-1 in cardioprotection: an insight with Glrx1 transgenic and knockout animals.
Identifieur interne : 000B71 ( Main/Exploration ); précédent : 000B70; suivant : 000B72Role of glutaredoxin-1 in cardioprotection: an insight with Glrx1 transgenic and knockout animals.
Auteurs : Gautam Malik [États-Unis] ; Norbert Nagy ; Ye-Shih Ho ; Nilanjana Maulik ; Dipak K. DasSource :
- Journal of molecular and cellular cardiology [ 1095-8584 ] ; 2008.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Apoptose (effets des médicaments et des substances chimiques), Chlorure de cadmium (pharmacologie), Contraction myocardique (effets des médicaments et des substances chimiques), Cytoprotection (effets des médicaments et des substances chimiques), Glutarédoxines (métabolisme), Humains (MeSH), Lésion de reperfusion myocardique (MeSH), Malonaldéhyde (métabolisme), Myocarde (anatomopathologie), Myocarde (cytologie), Myocarde (enzymologie), Myocarde (métabolisme), Myocytes cardiaques (cytologie), Myocytes cardiaques (effets des médicaments et des substances chimiques), Myocytes cardiaques (enzymologie), Phosphorylation (effets des médicaments et des substances chimiques), Protéines proto-oncogènes c-akt (métabolisme), Protéines proto-oncogènes c-bcl-2 (métabolisme), Rats (MeSH), Récupération fonctionnelle (effets des médicaments et des substances chimiques), Souris (MeSH), Souris knockout (MeSH), Stress oxydatif (effets des médicaments et des substances chimiques), Survie cellulaire (effets des médicaments et des substances chimiques), Techniques in vitro (MeSH).
- MESH :
- anatomopathologie : Myocarde.
- cytologie : Myocarde, Myocytes cardiaques.
- effets des médicaments et des substances chimiques : Apoptose, Contraction myocardique, Cytoprotection, Myocytes cardiaques, Phosphorylation, Récupération fonctionnelle, Stress oxydatif, Survie cellulaire.
- enzymologie : Myocarde, Myocytes cardiaques.
- métabolisme : Glutarédoxines, Malonaldéhyde, Myocarde, Protéines proto-oncogènes c-akt, Protéines proto-oncogènes c-bcl-2.
- pharmacologie : Chlorure de cadmium.
- Animaux, Humains, Lésion de reperfusion myocardique, Rats, Souris, Souris knockout, Techniques in vitro.
English descriptors
- KwdEn :
- Animals (MeSH), Apoptosis (drug effects), Cadmium Chloride (pharmacology), Cell Survival (drug effects), Cytoprotection (drug effects), Glutaredoxins (metabolism), Humans (MeSH), In Vitro Techniques (MeSH), Malondialdehyde (metabolism), Mice (MeSH), Mice, Knockout (MeSH), Myocardial Contraction (drug effects), Myocardial Reperfusion Injury (MeSH), Myocardium (cytology), Myocardium (enzymology), Myocardium (metabolism), Myocardium (pathology), Myocytes, Cardiac (cytology), Myocytes, Cardiac (drug effects), Myocytes, Cardiac (enzymology), Oxidative Stress (drug effects), Phosphorylation (drug effects), Proto-Oncogene Proteins c-akt (metabolism), Proto-Oncogene Proteins c-bcl-2 (metabolism), Rats (MeSH), Recovery of Function (drug effects).
- MESH :
- chemical , metabolism : Glutaredoxins, Malondialdehyde, Proto-Oncogene Proteins c-akt, Proto-Oncogene Proteins c-bcl-2.
- chemical , pharmacology : Cadmium Chloride.
- cytology : Myocardium, Myocytes, Cardiac.
- drug effects : Apoptosis, Cell Survival, Cytoprotection, Myocardial Contraction, Myocytes, Cardiac, Oxidative Stress, Phosphorylation, Recovery of Function.
- enzymology : Myocardium, Myocytes, Cardiac.
- metabolism : Myocardium.
- pathology : Myocardium.
- Animals, Humans, In Vitro Techniques, Mice, Mice, Knockout, Myocardial Reperfusion Injury, Rats.
Abstract
This study examined if glutaredoxin-1 (Glrx1), a redox-regulator of thioredoxin superfamily, plays any role in the redox signaling of ischemic myocardium. The hearts were subjected to 30 min of coronary occlusion followed by 24 h of reperfusion. Another group of hearts was rendered tolerant to ischemia (preconditioned, PC) by four cyclic episodes of 5 min ischemia each followed by another 10 min of reperfusion, which was then subjected to 30 min ischemia and 24 h of coronary occlusion. While ischemia/reperfusion had no effect on Glrx1 expression, adaptation to ischemia resulted in the up-regulation of Glrx1 expression, which was inhibited by cadmium, a known inhibitor of Glrx1. CdCl(2) also abolished cardioprotection afforded by PC as evidenced by its ability to partially increase myocardial infarct size without affecting cardiomyocyte apoptosis. The amount of ROS was significantly decreased in the PC heart, which was abolished by CdCl(2). The cardioprotective role of Glrx1was further confirmed with Glrx1 transgenic and knockout mice. The mouse hearts overexpressing Glrx1 exhibited significantly improved post-ischemic ventricular recovery and reduced myocardial infarct size while hearts deficient in Glrx1 exhibited depressed functional recovery and increased infarct size as compared to the wild-type hearts. Furthermore, Glrx1-overexpressing hearts exhibited reduced and Glrx1-deficient hearts exhibited increased ROS production during ischemia and reperfusion. Adapted hearts showed increased Akt phosphorylation that was inhibited by CdCl(2). The amount of Bcl-2 protein expression was not affected by the inhibition of Glrx1. Taken together, the results of this study implicate a role of Glrx1 in cardioprotection and redox signaling of the ischemic myocardium.
DOI: 10.1016/j.yjmcc.2007.08.022
PubMed: 17976641
Affiliations:
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Das</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="RBID">pubmed:17976641</idno><idno type="pmid">17976641</idno><idno type="doi">10.1016/j.yjmcc.2007.08.022</idno><idno type="wicri:Area/Main/Corpus">000C38</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000C38</idno><idno type="wicri:Area/Main/Curation">000C38</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000C38</idno><idno type="wicri:Area/Main/Exploration">000C38</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Role of glutaredoxin-1 in cardioprotection: an insight with Glrx1 transgenic and knockout animals.</title><author><name sortKey="Malik, Gautam" sort="Malik, Gautam" uniqKey="Malik G" first="Gautam" last="Malik">Gautam Malik</name><affiliation wicri:level="2"><nlm:affiliation>Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, Connecticut, CT 06030-1110, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, Connecticut, CT 06030-1110</wicri:regionArea><placeName><region type="state">Connecticut</region></placeName></affiliation></author><author><name sortKey="Nagy, Norbert" sort="Nagy, Norbert" uniqKey="Nagy N" first="Norbert" last="Nagy">Norbert Nagy</name></author><author><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name></author><author><name sortKey="Maulik, Nilanjana" sort="Maulik, Nilanjana" uniqKey="Maulik N" first="Nilanjana" last="Maulik">Nilanjana Maulik</name></author><author><name sortKey="Das, Dipak K" sort="Das, Dipak K" uniqKey="Das D" first="Dipak K" last="Das">Dipak K. Das</name></author></analytic><series><title level="j">Journal of molecular and cellular cardiology</title><idno type="eISSN">1095-8584</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Apoptosis (drug effects)</term><term>Cadmium Chloride (pharmacology)</term><term>Cell Survival (drug effects)</term><term>Cytoprotection (drug effects)</term><term>Glutaredoxins (metabolism)</term><term>Humans (MeSH)</term><term>In Vitro Techniques (MeSH)</term><term>Malondialdehyde (metabolism)</term><term>Mice (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Myocardial Contraction (drug effects)</term><term>Myocardial Reperfusion Injury (MeSH)</term><term>Myocardium (cytology)</term><term>Myocardium (enzymology)</term><term>Myocardium (metabolism)</term><term>Myocardium (pathology)</term><term>Myocytes, Cardiac (cytology)</term><term>Myocytes, Cardiac (drug effects)</term><term>Myocytes, Cardiac (enzymology)</term><term>Oxidative Stress (drug effects)</term><term>Phosphorylation (drug effects)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Proto-Oncogene Proteins c-bcl-2 (metabolism)</term><term>Rats (MeSH)</term><term>Recovery of Function (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Apoptose (effets des médicaments et des substances chimiques)</term><term>Chlorure de cadmium (pharmacologie)</term><term>Contraction myocardique (effets des médicaments et des substances chimiques)</term><term>Cytoprotection (effets des médicaments et des substances chimiques)</term><term>Glutarédoxines (métabolisme)</term><term>Humains (MeSH)</term><term>Lésion de reperfusion myocardique (MeSH)</term><term>Malonaldéhyde (métabolisme)</term><term>Myocarde (anatomopathologie)</term><term>Myocarde (cytologie)</term><term>Myocarde (enzymologie)</term><term>Myocarde (métabolisme)</term><term>Myocytes cardiaques (cytologie)</term><term>Myocytes cardiaques (effets des médicaments et des substances chimiques)</term><term>Myocytes cardiaques (enzymologie)</term><term>Phosphorylation (effets des médicaments et des substances chimiques)</term><term>Protéines proto-oncogènes c-akt (métabolisme)</term><term>Protéines proto-oncogènes c-bcl-2 (métabolisme)</term><term>Rats (MeSH)</term><term>Récupération fonctionnelle (effets des médicaments et des substances chimiques)</term><term>Souris (MeSH)</term><term>Souris knockout (MeSH)</term><term>Stress oxydatif (effets des médicaments et des substances chimiques)</term><term>Survie cellulaire (effets des médicaments et des substances chimiques)</term><term>Techniques in vitro (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutaredoxins</term><term>Malondialdehyde</term><term>Proto-Oncogene Proteins c-akt</term><term>Proto-Oncogene Proteins c-bcl-2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Cadmium Chloride</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Myocarde</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Myocarde</term><term>Myocytes cardiaques</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Myocardium</term><term>Myocytes, Cardiac</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Cell Survival</term><term>Cytoprotection</term><term>Myocardial Contraction</term><term>Myocytes, Cardiac</term><term>Oxidative Stress</term><term>Phosphorylation</term><term>Recovery of Function</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term><term>Contraction myocardique</term><term>Cytoprotection</term><term>Myocytes cardiaques</term><term>Phosphorylation</term><term>Récupération fonctionnelle</term><term>Stress oxydatif</term><term>Survie cellulaire</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Myocarde</term><term>Myocytes cardiaques</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Myocardium</term><term>Myocytes, Cardiac</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Myocardium</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Glutarédoxines</term><term>Malonaldéhyde</term><term>Myocarde</term><term>Protéines proto-oncogènes c-akt</term><term>Protéines proto-oncogènes c-bcl-2</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Myocardium</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Chlorure de cadmium</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>In Vitro Techniques</term><term>Mice</term><term>Mice, Knockout</term><term>Myocardial Reperfusion Injury</term><term>Rats</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Lésion de reperfusion myocardique</term><term>Rats</term><term>Souris</term><term>Souris knockout</term><term>Techniques in vitro</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">This study examined if glutaredoxin-1 (Glrx1), a redox-regulator of thioredoxin superfamily, plays any role in the redox signaling of ischemic myocardium. The hearts were subjected to 30 min of coronary occlusion followed by 24 h of reperfusion. Another group of hearts was rendered tolerant to ischemia (preconditioned, PC) by four cyclic episodes of 5 min ischemia each followed by another 10 min of reperfusion, which was then subjected to 30 min ischemia and 24 h of coronary occlusion. While ischemia/reperfusion had no effect on Glrx1 expression, adaptation to ischemia resulted in the up-regulation of Glrx1 expression, which was inhibited by cadmium, a known inhibitor of Glrx1. CdCl(2) also abolished cardioprotection afforded by PC as evidenced by its ability to partially increase myocardial infarct size without affecting cardiomyocyte apoptosis. The amount of ROS was significantly decreased in the PC heart, which was abolished by CdCl(2). The cardioprotective role of Glrx1was further confirmed with Glrx1 transgenic and knockout mice. The mouse hearts overexpressing Glrx1 exhibited significantly improved post-ischemic ventricular recovery and reduced myocardial infarct size while hearts deficient in Glrx1 exhibited depressed functional recovery and increased infarct size as compared to the wild-type hearts. Furthermore, Glrx1-overexpressing hearts exhibited reduced and Glrx1-deficient hearts exhibited increased ROS production during ischemia and reperfusion. Adapted hearts showed increased Akt phosphorylation that was inhibited by CdCl(2). The amount of Bcl-2 protein expression was not affected by the inhibition of Glrx1. Taken together, the results of this study implicate a role of Glrx1 in cardioprotection and redox signaling of the ischemic myocardium.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17976641</PMID><DateCompleted><Year>2008</Year><Month>04</Month><Day>03</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-8584</ISSN><JournalIssue CitedMedium="Internet"><Volume>44</Volume><Issue>2</Issue><PubDate><Year>2008</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Journal of molecular and cellular cardiology</Title><ISOAbbreviation>J Mol Cell Cardiol</ISOAbbreviation></Journal><ArticleTitle>Role of glutaredoxin-1 in cardioprotection: an insight with Glrx1 transgenic and knockout animals.</ArticleTitle><Pagination><MedlinePgn>261-9</MedlinePgn></Pagination><Abstract><AbstractText>This study examined if glutaredoxin-1 (Glrx1), a redox-regulator of thioredoxin superfamily, plays any role in the redox signaling of ischemic myocardium. The hearts were subjected to 30 min of coronary occlusion followed by 24 h of reperfusion. Another group of hearts was rendered tolerant to ischemia (preconditioned, PC) by four cyclic episodes of 5 min ischemia each followed by another 10 min of reperfusion, which was then subjected to 30 min ischemia and 24 h of coronary occlusion. While ischemia/reperfusion had no effect on Glrx1 expression, adaptation to ischemia resulted in the up-regulation of Glrx1 expression, which was inhibited by cadmium, a known inhibitor of Glrx1. CdCl(2) also abolished cardioprotection afforded by PC as evidenced by its ability to partially increase myocardial infarct size without affecting cardiomyocyte apoptosis. The amount of ROS was significantly decreased in the PC heart, which was abolished by CdCl(2). The cardioprotective role of Glrx1was further confirmed with Glrx1 transgenic and knockout mice. The mouse hearts overexpressing Glrx1 exhibited significantly improved post-ischemic ventricular recovery and reduced myocardial infarct size while hearts deficient in Glrx1 exhibited depressed functional recovery and increased infarct size as compared to the wild-type hearts. Furthermore, Glrx1-overexpressing hearts exhibited reduced and Glrx1-deficient hearts exhibited increased ROS production during ischemia and reperfusion. Adapted hearts showed increased Akt phosphorylation that was inhibited by CdCl(2). The amount of Bcl-2 protein expression was not affected by the inhibition of Glrx1. Taken together, the results of this study implicate a role of Glrx1 in cardioprotection and redox signaling of the ischemic myocardium.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Malik</LastName><ForeName>Gautam</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, Connecticut, CT 06030-1110, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nagy</LastName><ForeName>Norbert</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Ho</LastName><ForeName>Ye-Shih</ForeName><Initials>YS</Initials></Author><Author ValidYN="Y"><LastName>Maulik</LastName><ForeName>Nilanjana</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Das</LastName><ForeName>Dipak K</ForeName><Initials>DK</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>HL 34360</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL 85804</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL22559</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL33889</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL63317</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 ES06639</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016441">Retracted Publication</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>09</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Mol Cell Cardiol</MedlineTA><NlmUniqueID>0262322</NlmUniqueID><ISSNLinking>0022-2828</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019253">Proto-Oncogene Proteins c-bcl-2</NameOfSubstance></Chemical><Chemical><RegistryNumber>4Y8F71G49Q</RegistryNumber><NameOfSubstance UI="D008315">Malondialdehyde</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance></Chemical><Chemical><RegistryNumber>J6K4F9V3BA</RegistryNumber><NameOfSubstance UI="D019256">Cadmium Chloride</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="RetractionIn"><RefSource>J Mol Cell Cardiol. 2012 Nov;53(5):745</RefSource><PMID Version="1">23230606</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019256" MajorTopicYN="N">Cadmium Chloride</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019610" MajorTopicYN="Y">Cytoprotection</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066298" MajorTopicYN="N">In Vitro Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008315" MajorTopicYN="N">Malondialdehyde</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009200" MajorTopicYN="N">Myocardial Contraction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015428" MajorTopicYN="N">Myocardial Reperfusion Injury</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009206" MajorTopicYN="N">Myocardium</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019253" MajorTopicYN="N">Proto-Oncogene Proteins c-bcl-2</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020127" MajorTopicYN="N">Recovery of Function</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2007</Year><Month>07</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2007</Year><Month>08</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2007</Year><Month>08</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>11</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>4</Month><Day>4</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>11</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17976641</ArticleId><ArticleId IdType="pii">S0022-2828(07)01208-4</ArticleId><ArticleId IdType="doi">10.1016/j.yjmcc.2007.08.022</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Connecticut</li></region></list><tree><noCountry><name sortKey="Das, Dipak K" sort="Das, Dipak K" uniqKey="Das D" first="Dipak K" last="Das">Dipak K. Das</name><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name><name sortKey="Maulik, Nilanjana" sort="Maulik, Nilanjana" uniqKey="Maulik N" first="Nilanjana" last="Maulik">Nilanjana Maulik</name><name sortKey="Nagy, Norbert" sort="Nagy, Norbert" uniqKey="Nagy N" first="Norbert" last="Nagy">Norbert Nagy</name></noCountry><country name="États-Unis"><region name="Connecticut"><name sortKey="Malik, Gautam" sort="Malik, Gautam" uniqKey="Malik G" first="Gautam" last="Malik">Gautam Malik</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Role of glutaredoxin-1 in cardioprotection: an insight with Glrx1 transgenic and knockout animals.
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