GlutaredoxinV1, Main, Exploration, bibRecord, 000190

Cardiac-specific ablation of glutaredoxin 3 leads to cardiac hypertrophy and heart failure.

Identifieur interne : 000190 ( Main/Exploration ); précédent : 000189; suivant : 000191

Cardiac-specific ablation of glutaredoxin 3 leads to cardiac hypertrophy and heart failure.

Auteurs : Jimmonique Donelson [États-Unis] ; Qiongling Wang [États-Unis] ; Tanner O. Monroe [États-Unis] ; Xiqian Jiang [États-Unis] ; Jianjie Zhou [République populaire de Chine] ; Han Yu [États-Unis] ; Qianxing Mo [États-Unis] ; Qin Sun [États-Unis] ; Juan C. Marini [États-Unis] ; Xinquan Wang [République populaire de Chine] ; Paul A. Nakata [États-Unis] ; Kendal D. Hirschi [États-Unis] ; Jin Wang [États-Unis] ; George G. Rodney [États-Unis] ; Xander H T. Wehrens [États-Unis] ; Ninghui Cheng [États-Unis]

Source :

Physiological reports [ 2051-817X ] ; 2019.

RBID : pubmed:31033205

Descripteurs français

KwdFr :
- Animaux (MeSH), Cardiomégalie (génétique), Cardiomégalie (métabolisme), Cellules cultivées (MeSH), Défaillance cardiaque (génétique), Défaillance cardiaque (métabolisme), Espèces réactives de l'oxygène (métabolisme), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Myocytes cardiaques (métabolisme), Mâle (MeSH), Signalisation calcique (MeSH), Souris (MeSH), Stress oxydatif (MeSH), Vieillissement (anatomopathologie), Vieillissement (métabolisme).
MESH :
- anatomopathologie : Vieillissement.
- génétique : Cardiomégalie, Défaillance cardiaque, Glutarédoxines.
- métabolisme : Cardiomégalie, Défaillance cardiaque, Espèces réactives de l'oxygène, Glutarédoxines, Myocytes cardiaques, Vieillissement.
- Animaux, Cellules cultivées, Mâle, Signalisation calcique, Souris, Stress oxydatif.

English descriptors

KwdEn :
- Aging (metabolism), Aging (pathology), Animals (MeSH), Calcium Signaling (MeSH), Cardiomegaly (genetics), Cardiomegaly (metabolism), Cells, Cultured (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), Heart Failure (genetics), Heart Failure (metabolism), Male (MeSH), Mice (MeSH), Myocytes, Cardiac (metabolism), Oxidative Stress (MeSH), Reactive Oxygen Species (metabolism).
MESH :
- chemical , genetics : Glutaredoxins.
- genetics : Cardiomegaly, Heart Failure.
- metabolism : Aging, Cardiomegaly, Glutaredoxins, Heart Failure, Myocytes, Cardiac, Reactive Oxygen Species.
- pathology : Aging.
- Animals, Calcium Signaling, Cells, Cultured, Male, Mice, Oxidative Stress.

Abstract

Growing evidence suggests that redox-sensitive proteins including glutaredoxins (Grxs) can protect cardiac muscle cells from oxidative stress-induced damage. Mammalian Grx3 has been shown to be critical in regulating cellular redox states. However, how Grx3 affects cardiac function by modulating reactive oxygen species (ROS) signaling remains unknown. In this study, we found that the expression of Grx3 in the heart is decreased during aging. To assess the physiological role of Grx3 in the heart, we generated mice in which Grx3 was conditionally deleted in cardiomyocytes (Grx3 conditional knockout (CKO) mice). Grx3 CKO mice were viable and grew indistinguishably from their littermates at young age. No difference in cardiac function was found comparing Grx3 CKO mice and littermate controls at this age. However, by the age of 12 months, Grx3 CKO mice exhibited left ventricular hypertrophy with a significant decrease in ejection fraction and fractional shortening along with a significant increase of ROS production in cardiomyocytes compared to controls. Deletion of Grx3 also impaired Ca²⁺ handling, caused enhanced sarcoplasmic reticulum (SR) calcium (Ca²⁺ ) leak, and decreased SR Ca²⁺ uptake. Furthermore, enhanced ROS production and alteration of Ca²⁺ handling in cardiomyocytes occurred, prior to cardiac dysfunction in young mice. Therefore, our findings demonstrate that Grx3 is an important factor in regulating cardiac hypertrophy and heart failure by modulating both cellular redox homeostasis and Ca²⁺ handling in the heart.

DOI: 10.14814/phy2.14071
PubMed: 31033205
PubMed Central: PMC6487472

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<author><name sortKey="Wehrens, Xander H T" sort="Wehrens, Xander H T" uniqKey="Wehrens X" first="Xander H T" last="Wehrens">Xander H T. Wehrens</name>
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<author><name sortKey="Cheng, Ninghui" sort="Cheng, Ninghui" uniqKey="Cheng N" first="Ninghui" last="Cheng">Ninghui Cheng</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Cardiac-specific ablation of glutaredoxin 3 leads to cardiac hypertrophy and heart failure.</title>
<author><name sortKey="Donelson, Jimmonique" sort="Donelson, Jimmonique" uniqKey="Donelson J" first="Jimmonique" last="Donelson">Jimmonique Donelson</name>
<affiliation wicri:level="2"><nlm:affiliation>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
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<wicri:cityArea>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston</wicri:cityArea>
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<author><name sortKey="Wang, Qiongling" sort="Wang, Qiongling" uniqKey="Wang Q" first="Qiongling" last="Wang">Qiongling Wang</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
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<author><name sortKey="Monroe, Tanner O" sort="Monroe, Tanner O" uniqKey="Monroe T" first="Tanner O" last="Monroe">Tanner O. Monroe</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Jiang, Xiqian" sort="Jiang, Xiqian" uniqKey="Jiang X" first="Xiqian" last="Jiang">Xiqian Jiang</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Pharmacology and Chemical Biology, Baylor College of Medicine, Houston</wicri:cityArea>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
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<author><name sortKey="Zhou, Jianjie" sort="Zhou, Jianjie" uniqKey="Zhou J" first="Jianjie" last="Zhou">Jianjie Zhou</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Ministry of Education Key Laboratory of Protein Science, Center for Structural Biology, School of Life Sciences, Tsinghua University, Beijing</wicri:regionArea>
<placeName><settlement type="city">Pékin</settlement>
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<author><name sortKey="Yu, Han" sort="Yu, Han" uniqKey="Yu H" first="Han" last="Yu">Han Yu</name>
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<author><name sortKey="Mo, Qianxing" sort="Mo, Qianxing" uniqKey="Mo Q" first="Qianxing" last="Mo">Qianxing Mo</name>
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<placeName><region type="state">Floride</region>
</placeName>
<wicri:cityArea>Department of Biostatistics & Bioinformatics, H. Lee Moffitt Cancer Center & Research Institute, Tampa</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Sun, Qin" sort="Sun, Qin" uniqKey="Sun Q" first="Qin" last="Sun">Qin Sun</name>
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<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Molecular and Human Genetics, Baylor College of Medicine, Houston</wicri:cityArea>
</affiliation>
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<author><name sortKey="Marini, Juan C" sort="Marini, Juan C" uniqKey="Marini J" first="Juan C" last="Marini">Juan C. Marini</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston</wicri:cityArea>
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<affiliation wicri:level="2"><nlm:affiliation>Section of Critical Care Medicine, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Section of Critical Care Medicine, Department of Pediatrics, Baylor College of Medicine, Houston</wicri:cityArea>
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<author><name sortKey="Wang, Xinquan" sort="Wang, Xinquan" uniqKey="Wang X" first="Xinquan" last="Wang">Xinquan Wang</name>
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<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Ministry of Education Key Laboratory of Protein Science, Center for Structural Biology, School of Life Sciences, Tsinghua University, Beijing</wicri:regionArea>
<placeName><settlement type="city">Pékin</settlement>
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<author><name sortKey="Nakata, Paul A" sort="Nakata, Paul A" uniqKey="Nakata P" first="Paul A" last="Nakata">Paul A. Nakata</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Hirschi, Kendal D" sort="Hirschi, Kendal D" uniqKey="Hirschi K" first="Kendal D" last="Hirschi">Kendal D. Hirschi</name>
<affiliation wicri:level="2"><nlm:affiliation>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Wang, Jin" sort="Wang, Jin" uniqKey="Wang J" first="Jin" last="Wang">Jin Wang</name>
<affiliation wicri:level="2"><nlm:affiliation>Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, Texas.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Pharmacology and Chemical Biology, Baylor College of Medicine, Houston</wicri:cityArea>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Molecular and Cellular Biology, Baylor College of Medicine, Houston</wicri:cityArea>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Center for Drug Discovery, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Texas</region>
</placeName>
<wicri:cityArea>Center for Drug Discovery, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston</wicri:cityArea>
</affiliation>
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<author><name sortKey="Rodney, George G" sort="Rodney, George G" uniqKey="Rodney G" first="George G" last="Rodney">George G. Rodney</name>
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<author><name sortKey="Cheng, Ninghui" sort="Cheng, Ninghui" uniqKey="Cheng N" first="Ninghui" last="Cheng">Ninghui Cheng</name>
<affiliation wicri:level="2"><nlm:affiliation>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
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<series><title level="j">Physiological reports</title>
<idno type="eISSN">2051-817X</idno>
<imprint><date when="2019" type="published">2019</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aging (metabolism)</term>
<term>Aging (pathology)</term>
<term>Animals (MeSH)</term>
<term>Calcium Signaling (MeSH)</term>
<term>Cardiomegaly (genetics)</term>
<term>Cardiomegaly (metabolism)</term>
<term>Cells, Cultured (MeSH)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Heart Failure (genetics)</term>
<term>Heart Failure (metabolism)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Myocytes, Cardiac (metabolism)</term>
<term>Oxidative Stress (MeSH)</term>
<term>Reactive Oxygen Species (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Cardiomégalie (génétique)</term>
<term>Cardiomégalie (métabolisme)</term>
<term>Cellules cultivées (MeSH)</term>
<term>Défaillance cardiaque (génétique)</term>
<term>Défaillance cardiaque (métabolisme)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Myocytes cardiaques (métabolisme)</term>
<term>Mâle (MeSH)</term>
<term>Signalisation calcique (MeSH)</term>
<term>Souris (MeSH)</term>
<term>Stress oxydatif (MeSH)</term>
<term>Vieillissement (anatomopathologie)</term>
<term>Vieillissement (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Vieillissement</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cardiomegaly</term>
<term>Heart Failure</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Cardiomégalie</term>
<term>Défaillance cardiaque</term>
<term>Glutarédoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Aging</term>
<term>Cardiomegaly</term>
<term>Glutaredoxins</term>
<term>Heart Failure</term>
<term>Myocytes, Cardiac</term>
<term>Reactive Oxygen Species</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cardiomégalie</term>
<term>Défaillance cardiaque</term>
<term>Espèces réactives de l'oxygène</term>
<term>Glutarédoxines</term>
<term>Myocytes cardiaques</term>
<term>Vieillissement</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Aging</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Calcium Signaling</term>
<term>Cells, Cultured</term>
<term>Male</term>
<term>Mice</term>
<term>Oxidative Stress</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules cultivées</term>
<term>Mâle</term>
<term>Signalisation calcique</term>
<term>Souris</term>
<term>Stress oxydatif</term>
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<front><div type="abstract" xml:lang="en">Growing evidence suggests that redox-sensitive proteins including glutaredoxins (Grxs) can protect cardiac muscle cells from oxidative stress-induced damage. Mammalian Grx3 has been shown to be critical in regulating cellular redox states. However, how Grx3 affects cardiac function by modulating reactive oxygen species (ROS) signaling remains unknown. In this study, we found that the expression of Grx3 in the heart is decreased during aging. To assess the physiological role of Grx3 in the heart, we generated mice in which Grx3 was conditionally deleted in cardiomyocytes (Grx3 conditional knockout (CKO) mice). Grx3 CKO mice were viable and grew indistinguishably from their littermates at young age. No difference in cardiac function was found comparing Grx3 CKO mice and littermate controls at this age. However, by the age of 12 months, Grx3 CKO mice exhibited left ventricular hypertrophy with a significant decrease in ejection fraction and fractional shortening along with a significant increase of ROS production in cardiomyocytes compared to controls. Deletion of Grx3 also impaired Ca<sup>2+</sup>
 handling, caused enhanced sarcoplasmic reticulum (SR) calcium (Ca<sup>2+</sup>
 ) leak, and decreased SR Ca<sup>2+</sup>
 uptake. Furthermore, enhanced ROS production and alteration of Ca<sup>2+</sup>
 handling in cardiomyocytes occurred, prior to cardiac dysfunction in young mice. Therefore, our findings demonstrate that Grx3 is an important factor in regulating cardiac hypertrophy and heart failure by modulating both cellular redox homeostasis and Ca<sup>2+</sup>
 handling in the heart.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31033205</PMID>
<DateCompleted><Year>2020</Year>
<Month>04</Month>
<Day>30</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>10</Month>
<Day>09</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2051-817X</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>7</Volume>
<Issue>8</Issue>
<PubDate><Year>2019</Year>
<Month>04</Month>
</PubDate>
</JournalIssue>
<Title>Physiological reports</Title>
<ISOAbbreviation>Physiol Rep</ISOAbbreviation>
</Journal>
<ArticleTitle>Cardiac-specific ablation of glutaredoxin 3 leads to cardiac hypertrophy and heart failure.</ArticleTitle>
<Pagination><MedlinePgn>e14071</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.14814/phy2.14071</ELocationID>
<Abstract><AbstractText>Growing evidence suggests that redox-sensitive proteins including glutaredoxins (Grxs) can protect cardiac muscle cells from oxidative stress-induced damage. Mammalian Grx3 has been shown to be critical in regulating cellular redox states. However, how Grx3 affects cardiac function by modulating reactive oxygen species (ROS) signaling remains unknown. In this study, we found that the expression of Grx3 in the heart is decreased during aging. To assess the physiological role of Grx3 in the heart, we generated mice in which Grx3 was conditionally deleted in cardiomyocytes (Grx3 conditional knockout (CKO) mice). Grx3 CKO mice were viable and grew indistinguishably from their littermates at young age. No difference in cardiac function was found comparing Grx3 CKO mice and littermate controls at this age. However, by the age of 12 months, Grx3 CKO mice exhibited left ventricular hypertrophy with a significant decrease in ejection fraction and fractional shortening along with a significant increase of ROS production in cardiomyocytes compared to controls. Deletion of Grx3 also impaired Ca<sup>2+</sup>
 handling, caused enhanced sarcoplasmic reticulum (SR) calcium (Ca<sup>2+</sup>
 ) leak, and decreased SR Ca<sup>2+</sup>
 uptake. Furthermore, enhanced ROS production and alteration of Ca<sup>2+</sup>
 handling in cardiomyocytes occurred, prior to cardiac dysfunction in young mice. Therefore, our findings demonstrate that Grx3 is an important factor in regulating cardiac hypertrophy and heart failure by modulating both cellular redox homeostasis and Ca<sup>2+</sup>
 handling in the heart.</AbstractText>
<CopyrightInformation>© 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Donelson</LastName>
<ForeName>Jimmonique</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Qiongling</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>Molecular Physiology & Biophysics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Monroe</LastName>
<ForeName>Tanner O</ForeName>
<Initials>TO</Initials>
<AffiliationInfo><Affiliation>Molecular Physiology & Biophysics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jiang</LastName>
<ForeName>Xiqian</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhou</LastName>
<ForeName>Jianjie</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Ministry of Education Key Laboratory of Protein Science, Center for Structural Biology, School of Life Sciences, Tsinghua University, Beijing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yu</LastName>
<ForeName>Han</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mo</LastName>
<ForeName>Qianxing</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>Department of Biostatistics & Bioinformatics, H. Lee Moffitt Cancer Center & Research Institute, Tampa, Florida.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Qin</ForeName>
<Initials>Q</Initials>
<AffiliationInfo><Affiliation>Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Marini</LastName>
<ForeName>Juan C</ForeName>
<Initials>JC</Initials>
<AffiliationInfo><Affiliation>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Section of Critical Care Medicine, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Xinquan</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Ministry of Education Key Laboratory of Protein Science, Center for Structural Biology, School of Life Sciences, Tsinghua University, Beijing, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nakata</LastName>
<ForeName>Paul A</ForeName>
<Initials>PA</Initials>
<AffiliationInfo><Affiliation>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hirschi</LastName>
<ForeName>Kendal D</ForeName>
<Initials>KD</Initials>
<AffiliationInfo><Affiliation>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Jin</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Pharmacology and Chemical Biology, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Center for Drug Discovery, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rodney</LastName>
<ForeName>George G</ForeName>
<Initials>GG</Initials>
<AffiliationInfo><Affiliation>Molecular Physiology & Biophysics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wehrens</LastName>
<ForeName>Xander H T</ForeName>
<Initials>XHT</Initials>
<AffiliationInfo><Affiliation>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Molecular Physiology & Biophysics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cardiovascular Research Institute, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cheng</LastName>
<ForeName>Ninghui</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>USDA/ARS Children Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01-GM115622</GrantID>
<Acronym>NH</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01-HL089598</GrantID>
<Acronym>NH</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>13EIA14560061</GrantID>
<Acronym>AHA</Acronym>
<Agency>American Heart Association-American Stroke Association</Agency>
<Country>United States</Country>
</Grant>
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<Acronym>NH</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
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<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01-HL091947</GrantID>
<Acronym>NH</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01-HL117641</GrantID>
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<Country>United States</Country>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000375" MajorTopicYN="N">Aging</DescriptorName>
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<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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<MeshHeading><DescriptorName UI="D006332" MajorTopicYN="N">Cardiomegaly</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
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<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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</MeshHeading>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Calcium handling</Keyword>
<Keyword MajorTopicYN="Y">cardiac hypertrophy</Keyword>
<Keyword MajorTopicYN="Y">glutaredoxin</Keyword>
<Keyword MajorTopicYN="Y">heart failure</Keyword>
<Keyword MajorTopicYN="Y">oxidative stress</Keyword>
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Serveur d'exploration sur la glutarédoxine

Cardiac-specific ablation of glutaredoxin 3 leads to cardiac hypertrophy and heart failure.

Cardiac-specific ablation of glutaredoxin 3 leads to cardiac hypertrophy and heart failure.

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