GlutaredoxinV1, Main, Exploration, bibRecord, 000258

Glutaredoxin-2 controls cardiac mitochondrial dynamics and energetics in mice, and protects against human cardiac pathologies.

Identifieur interne : 000258 ( Main/Exploration ); précédent : 000257; suivant : 000259

Glutaredoxin-2 controls cardiac mitochondrial dynamics and energetics in mice, and protects against human cardiac pathologies.

Auteurs : Georges N. Kanaan [Canada] ; Bianca Ichim [Canada] ; Lara Gharibeh [Canada] ; Wael Maharsy [Canada] ; David A. Patten [Canada] ; Jian Ying Xuan [Canada] ; Arkadiy Reunov [Canada] ; Philip Marshall [Canada] ; John Veinot [Canada] ; Keir Menzies [Canada] ; Mona Nemer [Canada] ; Mary-Ellen Harper [Canada]

Source :

Redox biology [ 2213-2317 ] ; 2018.

RBID : pubmed:29101900

Descripteurs français

KwdFr :
- Acétylcystéine (usage thérapeutique), Animaux (MeSH), Cardiomégalie (anatomopathologie), Cardiomégalie (génétique), Cardiomégalie (métabolisme), Cardiomégalie (prévention et contrôle), Cardiopathies (anatomopathologie), Cardiopathies (génétique), Cardiopathies (métabolisme), Cardiopathies (prévention et contrôle), Cellules cultivées (MeSH), Dynamique mitochondriale (MeSH), Facteurs de protection (MeSH), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Humains (MeSH), Mitochondries (anatomopathologie), Mitochondries (métabolisme), Mâle (MeSH), Métabolisme énergétique (MeSH), Oxydoréduction (MeSH), Souris (MeSH), Souris de lignée C57BL (MeSH), Souris knockout (MeSH), Stress oxydatif (MeSH).
MESH :
- anatomopathologie : Cardiomégalie, Cardiopathies, Mitochondries.
- génétique : Cardiomégalie, Cardiopathies, Glutarédoxines.
- métabolisme : Cardiomégalie, Cardiopathies, Glutarédoxines, Mitochondries.
- prévention et contrôle : Cardiomégalie, Cardiopathies.
- usage thérapeutique : Acétylcystéine.
- Animaux, Cellules cultivées, Dynamique mitochondriale, Facteurs de protection, Humains, Mâle, Métabolisme énergétique, Oxydoréduction, Souris, Souris de lignée C57BL, Souris knockout, Stress oxydatif.

English descriptors

KwdEn :
- Acetylcysteine (therapeutic use), Animals (MeSH), Cardiomegaly (genetics), Cardiomegaly (metabolism), Cardiomegaly (pathology), Cardiomegaly (prevention & control), Cells, Cultured (MeSH), Energy Metabolism (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), Heart Diseases (genetics), Heart Diseases (metabolism), Heart Diseases (pathology), Heart Diseases (prevention & control), Humans (MeSH), Male (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), Mitochondria (metabolism), Mitochondria (pathology), Mitochondrial Dynamics (MeSH), Oxidation-Reduction (MeSH), Oxidative Stress (MeSH), Protective Factors (MeSH).
MESH :
- chemical , genetics : Glutaredoxins.
- chemical , metabolism : Glutaredoxins.
- chemical , therapeutic use : Acetylcysteine.
- genetics : Cardiomegaly, Heart Diseases.
- metabolism : Cardiomegaly, Heart Diseases, Mitochondria.
- pathology : Cardiomegaly, Heart Diseases, Mitochondria.
- prevention & control : Cardiomegaly, Heart Diseases.
- Animals, Cells, Cultured, Energy Metabolism, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitochondrial Dynamics, Oxidation-Reduction, Oxidative Stress, Protective Factors.

Abstract

Glutaredoxin 2 (GRX2), a mitochondrial glutathione-dependent oxidoreductase, is central to glutathione homeostasis and mitochondrial redox, which is crucial in highly metabolic tissues like the heart. Previous research showed that absence of Grx2, leads to impaired mitochondrial complex I function, hypertension and cardiac hypertrophy in mice but the impact on mitochondrial structure and function in intact cardiomyocytes and in humans has not been explored. We hypothesized that Grx2 controls cardiac mitochondrial dynamics and function in cellular and mouse models, and that low expression is associated with human cardiac dysfunction. Here we show that Grx2 absence impairs mitochondrial fusion, ultrastructure and energetics in primary cardiomyocytes and cardiac tissue. Moreover, provision of the glutathione precursor, N-acetylcysteine (NAC) to Grx2-/- mice did not restore glutathione redox or prevent impairments. Using genetic and histopathological data from the human Genotype-Tissue Expression consortium we demonstrate that low GRX2 is associated with fibrosis, hypertrophy, and infarct in the left ventricle. Altogether, GRX2 is important in the control of cardiac mitochondrial structure and function, and protects against human cardiac pathologies.

DOI: 10.1016/j.redox.2017.10.019
PubMed: 29101900
PubMed Central: PMC5675898

Affiliations:

Canada

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Le document en format XML

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</affiliation>
</author>
<author><name sortKey="Harper, Mary Ellen" sort="Harper, Mary Ellen" uniqKey="Harper M" first="Mary-Ellen" last="Harper">Mary-Ellen Harper</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Glutaredoxin-2 controls cardiac mitochondrial dynamics and energetics in mice, and protects against human cardiac pathologies.</title>
<author><name sortKey="Kanaan, Georges N" sort="Kanaan, Georges N" uniqKey="Kanaan G" first="Georges N" last="Kanaan">Georges N. Kanaan</name>
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<wicri:noRegion>ON</wicri:noRegion>
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</author>
<author><name sortKey="Ichim, Bianca" sort="Ichim, Bianca" uniqKey="Ichim B" first="Bianca" last="Ichim">Bianca Ichim</name>
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<author><name sortKey="Gharibeh, Lara" sort="Gharibeh, Lara" uniqKey="Gharibeh L" first="Lara" last="Gharibeh">Lara Gharibeh</name>
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<author><name sortKey="Patten, David A" sort="Patten, David A" uniqKey="Patten D" first="David A" last="Patten">David A. Patten</name>
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<wicri:noRegion>ON</wicri:noRegion>
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</author>
<author><name sortKey="Xuan, Jian Ying" sort="Xuan, Jian Ying" uniqKey="Xuan J" first="Jian Ying" last="Xuan">Jian Ying Xuan</name>
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<country>Canada</country>
<wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON</wicri:regionArea>
<wicri:noRegion>ON</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Reunov, Arkadiy" sort="Reunov, Arkadiy" uniqKey="Reunov A" first="Arkadiy" last="Reunov">Arkadiy Reunov</name>
<affiliation wicri:level="1"><nlm:affiliation>Ottawa Heart Institute, University of Ottawa, 40 Ruskin Street, Ottawa, ON, Canada K1Y 4W7.</nlm:affiliation>
<country>Canada</country>
<wicri:regionArea>Ottawa Heart Institute, University of Ottawa, 40 Ruskin Street, Ottawa, ON</wicri:regionArea>
<wicri:noRegion>ON</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Marshall, Philip" sort="Marshall, Philip" uniqKey="Marshall P" first="Philip" last="Marshall">Philip Marshall</name>
<affiliation wicri:level="1"><nlm:affiliation>Interdisciplinary School of Health Sciences, University of Ottawa, Faculty of Health Sciences, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</nlm:affiliation>
<country>Canada</country>
<wicri:regionArea>Interdisciplinary School of Health Sciences, University of Ottawa, Faculty of Health Sciences, 451 Smyth Road, Ottawa, ON</wicri:regionArea>
<wicri:noRegion>ON</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Veinot, John" sort="Veinot, John" uniqKey="Veinot J" first="John" last="Veinot">John Veinot</name>
<affiliation wicri:level="1"><nlm:affiliation>Ottawa Heart Institute, University of Ottawa, 40 Ruskin Street, Ottawa, ON, Canada K1Y 4W7; The Ottawa Hospital, 501 Smyth Road, Ottawa, ON, Canada K1H8L6; Department of Pathology and Laboratory Medicine, and University of Ottawa, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</nlm:affiliation>
<country>Canada</country>
<wicri:regionArea>Ottawa Heart Institute, University of Ottawa, 40 Ruskin Street, Ottawa, ON, Canada K1Y 4W7; The Ottawa Hospital, 501 Smyth Road, Ottawa, ON, Canada K1H8L6; Department of Pathology and Laboratory Medicine, and University of Ottawa, Faculty of Medicine, 451 Smyth Road, Ottawa, ON</wicri:regionArea>
<wicri:noRegion>ON</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Menzies, Keir" sort="Menzies, Keir" uniqKey="Menzies K" first="Keir" last="Menzies">Keir Menzies</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5; Interdisciplinary School of Health Sciences, University of Ottawa, Faculty of Health Sciences, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</nlm:affiliation>
<country>Canada</country>
<wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5; Interdisciplinary School of Health Sciences, University of Ottawa, Faculty of Health Sciences, 451 Smyth Road, Ottawa, ON</wicri:regionArea>
<wicri:noRegion>ON</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Nemer, Mona" sort="Nemer, Mona" uniqKey="Nemer M" first="Mona" last="Nemer">Mona Nemer</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</nlm:affiliation>
<country>Canada</country>
<wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON</wicri:regionArea>
<wicri:noRegion>ON</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Harper, Mary Ellen" sort="Harper, Mary Ellen" uniqKey="Harper M" first="Mary-Ellen" last="Harper">Mary-Ellen Harper</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5. Electronic address: mharper@uottawa.ca.</nlm:affiliation>
<country>Canada</country>
<wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON</wicri:regionArea>
<wicri:noRegion>ON</wicri:noRegion>
</affiliation>
</author>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylcysteine (therapeutic use)</term>
<term>Animals (MeSH)</term>
<term>Cardiomegaly (genetics)</term>
<term>Cardiomegaly (metabolism)</term>
<term>Cardiomegaly (pathology)</term>
<term>Cardiomegaly (prevention & control)</term>
<term>Cells, Cultured (MeSH)</term>
<term>Energy Metabolism (MeSH)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Heart Diseases (genetics)</term>
<term>Heart Diseases (metabolism)</term>
<term>Heart Diseases (pathology)</term>
<term>Heart Diseases (prevention & control)</term>
<term>Humans (MeSH)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Mitochondria (metabolism)</term>
<term>Mitochondria (pathology)</term>
<term>Mitochondrial Dynamics (MeSH)</term>
<term>Oxidation-Reduction (MeSH)</term>
<term>Oxidative Stress (MeSH)</term>
<term>Protective Factors (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Acétylcystéine (usage thérapeutique)</term>
<term>Animaux (MeSH)</term>
<term>Cardiomégalie (anatomopathologie)</term>
<term>Cardiomégalie (génétique)</term>
<term>Cardiomégalie (métabolisme)</term>
<term>Cardiomégalie (prévention et contrôle)</term>
<term>Cardiopathies (anatomopathologie)</term>
<term>Cardiopathies (génétique)</term>
<term>Cardiopathies (métabolisme)</term>
<term>Cardiopathies (prévention et contrôle)</term>
<term>Cellules cultivées (MeSH)</term>
<term>Dynamique mitochondriale (MeSH)</term>
<term>Facteurs de protection (MeSH)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Mitochondries (anatomopathologie)</term>
<term>Mitochondries (métabolisme)</term>
<term>Mâle (MeSH)</term>
<term>Métabolisme énergétique (MeSH)</term>
<term>Oxydoréduction (MeSH)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Souris knockout (MeSH)</term>
<term>Stress oxydatif (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutaredoxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Acetylcysteine</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cardiomégalie</term>
<term>Cardiopathies</term>
<term>Mitochondries</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cardiomegaly</term>
<term>Heart Diseases</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cardiomégalie</term>
<term>Cardiopathies</term>
<term>Glutarédoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cardiomegaly</term>
<term>Heart Diseases</term>
<term>Mitochondria</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cardiomégalie</term>
<term>Cardiopathies</term>
<term>Glutarédoxines</term>
<term>Mitochondries</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cardiomegaly</term>
<term>Heart Diseases</term>
<term>Mitochondria</term>
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<term>Cells, Cultured</term>
<term>Energy Metabolism</term>
<term>Humans</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Mitochondrial Dynamics</term>
<term>Oxidation-Reduction</term>
<term>Oxidative Stress</term>
<term>Protective Factors</term>
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<term>Dynamique mitochondriale</term>
<term>Facteurs de protection</term>
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<term>Mâle</term>
<term>Métabolisme énergétique</term>
<term>Oxydoréduction</term>
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<front><div type="abstract" xml:lang="en">Glutaredoxin 2 (GRX2), a mitochondrial glutathione-dependent oxidoreductase, is central to glutathione homeostasis and mitochondrial redox, which is crucial in highly metabolic tissues like the heart. Previous research showed that absence of Grx2, leads to impaired mitochondrial complex I function, hypertension and cardiac hypertrophy in mice but the impact on mitochondrial structure and function in intact cardiomyocytes and in humans has not been explored. We hypothesized that Grx2 controls cardiac mitochondrial dynamics and function in cellular and mouse models, and that low expression is associated with human cardiac dysfunction. Here we show that Grx2 absence impairs mitochondrial fusion, ultrastructure and energetics in primary cardiomyocytes and cardiac tissue. Moreover, provision of the glutathione precursor, N-acetylcysteine (NAC) to Grx2-/- mice did not restore glutathione redox or prevent impairments. Using genetic and histopathological data from the human Genotype-Tissue Expression consortium we demonstrate that low GRX2 is associated with fibrosis, hypertrophy, and infarct in the left ventricle. Altogether, GRX2 is important in the control of cardiac mitochondrial structure and function, and protects against human cardiac pathologies.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29101900</PMID>
<DateCompleted><Year>2018</Year>
<Month>07</Month>
<Day>16</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2213-2317</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>14</Volume>
<PubDate><Year>2018</Year>
<Month>04</Month>
</PubDate>
</JournalIssue>
<Title>Redox biology</Title>
<ISOAbbreviation>Redox Biol</ISOAbbreviation>
</Journal>
<ArticleTitle>Glutaredoxin-2 controls cardiac mitochondrial dynamics and energetics in mice, and protects against human cardiac pathologies.</ArticleTitle>
<Pagination><MedlinePgn>509-521</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S2213-2317(17)30806-6</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.redox.2017.10.019</ELocationID>
<Abstract><AbstractText>Glutaredoxin 2 (GRX2), a mitochondrial glutathione-dependent oxidoreductase, is central to glutathione homeostasis and mitochondrial redox, which is crucial in highly metabolic tissues like the heart. Previous research showed that absence of Grx2, leads to impaired mitochondrial complex I function, hypertension and cardiac hypertrophy in mice but the impact on mitochondrial structure and function in intact cardiomyocytes and in humans has not been explored. We hypothesized that Grx2 controls cardiac mitochondrial dynamics and function in cellular and mouse models, and that low expression is associated with human cardiac dysfunction. Here we show that Grx2 absence impairs mitochondrial fusion, ultrastructure and energetics in primary cardiomyocytes and cardiac tissue. Moreover, provision of the glutathione precursor, N-acetylcysteine (NAC) to Grx2-/- mice did not restore glutathione redox or prevent impairments. Using genetic and histopathological data from the human Genotype-Tissue Expression consortium we demonstrate that low GRX2 is associated with fibrosis, hypertrophy, and infarct in the left ventricle. Altogether, GRX2 is important in the control of cardiac mitochondrial structure and function, and protects against human cardiac pathologies.</AbstractText>
<CopyrightInformation>Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kanaan</LastName>
<ForeName>Georges N</ForeName>
<Initials>GN</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ichim</LastName>
<ForeName>Bianca</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gharibeh</LastName>
<ForeName>Lara</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Maharsy</LastName>
<ForeName>Wael</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Patten</LastName>
<ForeName>David A</ForeName>
<Initials>DA</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xuan</LastName>
<ForeName>Jian Ying</ForeName>
<Initials>JY</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Reunov</LastName>
<ForeName>Arkadiy</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Ottawa Heart Institute, University of Ottawa, 40 Ruskin Street, Ottawa, ON, Canada K1Y 4W7.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Marshall</LastName>
<ForeName>Philip</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Interdisciplinary School of Health Sciences, University of Ottawa, Faculty of Health Sciences, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Veinot</LastName>
<ForeName>John</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Ottawa Heart Institute, University of Ottawa, 40 Ruskin Street, Ottawa, ON, Canada K1Y 4W7; The Ottawa Hospital, 501 Smyth Road, Ottawa, ON, Canada K1H8L6; Department of Pathology and Laboratory Medicine, and University of Ottawa, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Menzies</LastName>
<ForeName>Keir</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5; Interdisciplinary School of Health Sciences, University of Ottawa, Faculty of Health Sciences, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nemer</LastName>
<ForeName>Mona</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Harper</LastName>
<ForeName>Mary-Ellen</ForeName>
<Initials>ME</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, and Ottawa Institute of Systems Biology, Faculty of Medicine, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5. Electronic address: mharper@uottawa.ca.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>FDN 143278</GrantID>
<Agency>CIHR</Agency>
<Country>Canada</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>10</Month>
<Day>26</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>Redox Biol</MedlineTA>
<NlmUniqueID>101605639</NlmUniqueID>
<ISSNLinking>2213-2317</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>WYQ7N0BPYC</RegistryNumber>
<NameOfSubstance UI="D000111">Acetylcysteine</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000111" MajorTopicYN="N">Acetylcysteine</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006332" MajorTopicYN="N">Cardiomegaly</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004734" MajorTopicYN="Y">Energy Metabolism</DescriptorName>
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<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
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<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D063154" MajorTopicYN="Y">Mitochondrial Dynamics</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D065840" MajorTopicYN="N">Protective Factors</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Cardiac hypertrophy</Keyword>
<Keyword MajorTopicYN="Y">Cardiac metabolism</Keyword>
<Keyword MajorTopicYN="Y">Human heart</Keyword>
<Keyword MajorTopicYN="Y">Mitochondria</Keyword>
<Keyword MajorTopicYN="Y">Oxidative stress</Keyword>
<Keyword MajorTopicYN="Y">Redox</Keyword>
</KeywordList>
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EXPLOR_STEP=$WICRI_ROOT/Bois/explor/GlutaredoxinV1/Data/Main/Exploration

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000258 | SxmlIndent | more

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{{Explor lien
   |wiki=    Bois
   |area=    GlutaredoxinV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:29101900
   |texte=   Glutaredoxin-2 controls cardiac mitochondrial dynamics and energetics in mice, and protects against human cardiac pathologies.
}}

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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:29101900" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a GlutaredoxinV1

This area was generated with Dilib version V0.6.37.
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	Serveur d'exploration sur la glutarédoxine
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Serveur d'exploration sur la glutarédoxine

Glutaredoxin-2 controls cardiac mitochondrial dynamics and energetics in mice, and protects against human cardiac pathologies.

Glutaredoxin-2 controls cardiac mitochondrial dynamics and energetics in mice, and protects against human cardiac pathologies.

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