IronSulferCluV1, Main, Exploration, bibRecord, 000054

Pharmacological Silencing of MicroRNA-152 Prevents Pressure Overload-Induced Heart Failure.

Identifieur interne : 000054 ( Main/Exploration ); précédent : 000053; suivant : 000055

Pharmacological Silencing of MicroRNA-152 Prevents Pressure Overload-Induced Heart Failure.

Auteurs : Thomas J. Larocca [États-Unis] ; Timon Seeger [États-Unis] ; Maricela Prado [États-Unis] ; Isaac Perea-Gil [États-Unis] ; Evgenios Neofytou [États-Unis] ; Brigham H. Mecham ; Mohamed Ameen [États-Unis] ; Alex Chia Yu Chang ; Gaurav Pandey ; Joseph C. Wu [États-Unis] ; Ioannis Karakikes [États-Unis]

Source :

Circulation. Heart failure [ 1941-3297 ] ; 2020.

RBID : pubmed:32160771

Descripteurs français

KwdFr :
- Animaux (MeSH), Antagomirs (administration et posologie), Aorte (chirurgie), Aorte (physiopathologie), Débit systolique (MeSH), Défaillance cardiaque (génétique), Défaillance cardiaque (métabolisme), Défaillance cardiaque (physiopathologie), Défaillance cardiaque (prévention et contrôle), Extinction de l'expression des gènes (MeSH), Fonction ventriculaire gauche (MeSH), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Humains (MeSH), Ligature (MeSH), Mitochondries du myocarde (génétique), Mitochondries du myocarde (métabolisme), Mitochondries du myocarde (ultrastructure), Modèles animaux de maladie humaine (MeSH), Myocytes cardiaques (métabolisme), Myocytes cardiaques (ultrastructure), Mâle (MeSH), Souris de lignée C57BL (MeSH), Souris transgéniques (MeSH), microARN (génétique), microARN (métabolisme), Étude de validation de principe (MeSH), Études cas-témoins (MeSH).
MESH :
- administration et posologie : Antagomirs.
- chirurgie : Aorte.
- génétique : Défaillance cardiaque, Glutarédoxines, Mitochondries du myocarde, microARN.
- métabolisme : Défaillance cardiaque, Glutarédoxines, Mitochondries du myocarde, Myocytes cardiaques, microARN.
- physiopathologie : Aorte, Défaillance cardiaque.
- prévention et contrôle : Défaillance cardiaque.
- ultrastructure : Animaux, Débit systolique, Extinction de l'expression des gènes, Fonction ventriculaire gauche, Humains, Ligature, Mitochondries du myocarde, Modèles animaux de maladie humaine, Myocytes cardiaques, Mâle, Souris de lignée C57BL, Souris transgéniques, Étude de validation de principe, Études cas-témoins.

English descriptors

KwdEn :
- Animals (MeSH), Antagomirs (administration & dosage), Aorta (physiopathology), Aorta (surgery), Case-Control Studies (MeSH), Disease Models, Animal (MeSH), Gene Silencing (MeSH), Glutaredoxins (genetics), Glutaredoxins (metabolism), Heart Failure (genetics), Heart Failure (metabolism), Heart Failure (physiopathology), Heart Failure (prevention & control), Humans (MeSH), Ligation (MeSH), Male (MeSH), Mice, Inbred C57BL (MeSH), Mice, Transgenic (MeSH), MicroRNAs (genetics), MicroRNAs (metabolism), Mitochondria, Heart (genetics), Mitochondria, Heart (metabolism), Mitochondria, Heart (ultrastructure), Myocytes, Cardiac (metabolism), Myocytes, Cardiac (ultrastructure), Proof of Concept Study (MeSH), Stroke Volume (MeSH), Ventricular Function, Left (MeSH).
MESH :
- chemical , administration & dosage : Antagomirs.
- chemical , genetics : Glutaredoxins, MicroRNAs.
- chemical , metabolism : Glutaredoxins, MicroRNAs.
- genetics : Heart Failure, Mitochondria, Heart.
- metabolism : Heart Failure, Mitochondria, Heart, Myocytes, Cardiac.
- physiopathology : Aorta, Heart Failure.
- prevention & control : Heart Failure.
- surgery : Aorta.
- ultrastructure : Mitochondria, Heart, Myocytes, Cardiac.
- Animals, Case-Control Studies, Disease Models, Animal, Gene Silencing, Humans, Ligation, Male, Mice, Inbred C57BL, Mice, Transgenic, Proof of Concept Study, Stroke Volume, Ventricular Function, Left.

Abstract

BACKGROUND

MicroRNAs are small, noncoding RNAs that play a key role in gene expression. Accumulating evidence suggests that aberrant microRNA expression contributes to the heart failure (HF) phenotype; however, the underlying molecular mechanisms are not well understood. A better understanding of the mechanisms of action of microRNAs could potentially lead to targeted therapies that could halt the progression or even reverse HF.

METHODS AND RESULTS

We found that microRNA-152 (miR-152) expression was upregulated in the failing human heart and experimental animal models of HF. Transgenic mice with cardiomyocyte-specific miR-152 overexpression developed systolic dysfunction (mean difference, -38.74% [95% CI, -45.73% to -31.74%];

CONCLUSIONS

The upregulation of miR-152 expression in the failing myocardium contributes to HF pathophysiology. Preclinical evidence suggests that miR-152 inhibition preserves cardiac function in a model of pressure overload-induced HF. These findings offer new insights into the pathophysiology of HF and point to miR-152-Glrx5 axis as a potential novel therapeutic target.

DOI: 10.1161/CIRCHEARTFAILURE.119.006298
PubMed: 32160771
PubMed Central: PMC7439562

Affiliations:

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

to stream Main, to step Corpus: 000128
to stream Main, to step Curation: 000128

Le document en format XML

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<author><name sortKey="Larocca, Thomas J" sort="Larocca, Thomas J" uniqKey="Larocca T" first="Thomas J" last="Larocca">Thomas J. Larocca</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Critical Care Medicine, Department of Pediatrics, Lucile Packard Children's Hospital (T.J.L.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Perea Gil, Isaac" sort="Perea Gil, Isaac" uniqKey="Perea Gil I" first="Isaac" last="Perea-Gil">Isaac Perea-Gil</name>
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<author><name sortKey="Neofytou, Evgenios" sort="Neofytou, Evgenios" uniqKey="Neofytou E" first="Evgenios" last="Neofytou">Evgenios Neofytou</name>
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<author><name sortKey="Mecham, Brigham H" sort="Mecham, Brigham H" uniqKey="Mecham B" first="Brigham H" last="Mecham">Brigham H. Mecham</name>
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<wicri:noCountry code="subField">WA (B.H.M.).</wicri:noCountry>
</affiliation>
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<author><name sortKey="Ameen, Mohamed" sort="Ameen, Mohamed" uniqKey="Ameen M" first="Mohamed" last="Ameen">Mohamed Ameen</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Chang, Alex Chia Yu" sort="Chang, Alex Chia Yu" uniqKey="Chang A" first="Alex Chia Yu" last="Chang">Alex Chia Yu Chang</name>
<affiliation><nlm:affiliation>Department of Cardiology and Shanghai Institute of Precision Medicine, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, China (A.C.Y.C.).</nlm:affiliation>
<wicri:noCountry code="subField">China (A.C.Y.C.).</wicri:noCountry>
</affiliation>
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<author><name sortKey="Pandey, Gaurav" sort="Pandey, Gaurav" uniqKey="Pandey G" first="Gaurav" last="Pandey">Gaurav Pandey</name>
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<wicri:noCountry code="subField">NY (G.P.).</wicri:noCountry>
</affiliation>
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<author><name sortKey="Wu, Joseph C" sort="Wu, Joseph C" uniqKey="Wu J" first="Joseph C" last="Wu">Joseph C. Wu</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
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<affiliation wicri:level="2"><nlm:affiliation>Department of Radiology (J.C.W.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
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</affiliation>
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<author><name sortKey="Karakikes, Ioannis" sort="Karakikes, Ioannis" uniqKey="Karakikes I" first="Ioannis" last="Karakikes">Ioannis Karakikes</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Cardiothoracic Surgery (M.P., I.P.-G., I.K.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Department of Cardiothoracic Surgery (M.P., I.P.-G., I.K.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Pharmacological Silencing of MicroRNA-152 Prevents Pressure Overload-Induced Heart Failure.</title>
<author><name sortKey="Larocca, Thomas J" sort="Larocca, Thomas J" uniqKey="Larocca T" first="Thomas J" last="Larocca">Thomas J. Larocca</name>
<affiliation wicri:level="2"><nlm:affiliation>Division of Critical Care Medicine, Department of Pediatrics, Lucile Packard Children's Hospital (T.J.L.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Division of Critical Care Medicine, Department of Pediatrics, Lucile Packard Children's Hospital (T.J.L.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Seeger, Timon" sort="Seeger, Timon" uniqKey="Seeger T" first="Timon" last="Seeger">Timon Seeger</name>
<affiliation wicri:level="2"><nlm:affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Prado, Maricela" sort="Prado, Maricela" uniqKey="Prado M" first="Maricela" last="Prado">Maricela Prado</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Cardiothoracic Surgery (M.P., I.P.-G., I.K.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Department of Cardiothoracic Surgery (M.P., I.P.-G., I.K.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Perea Gil, Isaac" sort="Perea Gil, Isaac" uniqKey="Perea Gil I" first="Isaac" last="Perea-Gil">Isaac Perea-Gil</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Cardiothoracic Surgery (M.P., I.P.-G., I.K.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Department of Cardiothoracic Surgery (M.P., I.P.-G., I.K.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Neofytou, Evgenios" sort="Neofytou, Evgenios" uniqKey="Neofytou E" first="Evgenios" last="Neofytou">Evgenios Neofytou</name>
<affiliation wicri:level="2"><nlm:affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Mecham, Brigham H" sort="Mecham, Brigham H" uniqKey="Mecham B" first="Brigham H" last="Mecham">Brigham H. Mecham</name>
<affiliation><nlm:affiliation>Trialomics, LLC, Seattle, WA (B.H.M.).</nlm:affiliation>
<wicri:noCountry code="subField">WA (B.H.M.).</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Ameen, Mohamed" sort="Ameen, Mohamed" uniqKey="Ameen M" first="Mohamed" last="Ameen">Mohamed Ameen</name>
<affiliation wicri:level="2"><nlm:affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Chang, Alex Chia Yu" sort="Chang, Alex Chia Yu" uniqKey="Chang A" first="Alex Chia Yu" last="Chang">Alex Chia Yu Chang</name>
<affiliation><nlm:affiliation>Department of Cardiology and Shanghai Institute of Precision Medicine, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, China (A.C.Y.C.).</nlm:affiliation>
<wicri:noCountry code="subField">China (A.C.Y.C.).</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Pandey, Gaurav" sort="Pandey, Gaurav" uniqKey="Pandey G" first="Gaurav" last="Pandey">Gaurav Pandey</name>
<affiliation><nlm:affiliation>Department of Genetics and Genomic Sciences, Icahn Institute of Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY (G.P.).</nlm:affiliation>
<wicri:noCountry code="subField">NY (G.P.).</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Wu, Joseph C" sort="Wu, Joseph C" uniqKey="Wu J" first="Joseph C" last="Wu">Joseph C. Wu</name>
<affiliation wicri:level="2"><nlm:affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Department of Radiology (J.C.W.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Department of Radiology (J.C.W.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Karakikes, Ioannis" sort="Karakikes, Ioannis" uniqKey="Karakikes I" first="Ioannis" last="Karakikes">Ioannis Karakikes</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Cardiothoracic Surgery (M.P., I.P.-G., I.K.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Department of Cardiothoracic Surgery (M.P., I.P.-G., I.K.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine</wicri:cityArea>
</affiliation>
</author>
</analytic>
<series><title level="j">Circulation. Heart failure</title>
<idno type="eISSN">1941-3297</idno>
<imprint><date when="2020" type="published">2020</date>
</imprint>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Antagomirs (administration & dosage)</term>
<term>Aorta (physiopathology)</term>
<term>Aorta (surgery)</term>
<term>Case-Control Studies (MeSH)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Gene Silencing (MeSH)</term>
<term>Glutaredoxins (genetics)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Heart Failure (genetics)</term>
<term>Heart Failure (metabolism)</term>
<term>Heart Failure (physiopathology)</term>
<term>Heart Failure (prevention & control)</term>
<term>Humans (MeSH)</term>
<term>Ligation (MeSH)</term>
<term>Male (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mice, Transgenic (MeSH)</term>
<term>MicroRNAs (genetics)</term>
<term>MicroRNAs (metabolism)</term>
<term>Mitochondria, Heart (genetics)</term>
<term>Mitochondria, Heart (metabolism)</term>
<term>Mitochondria, Heart (ultrastructure)</term>
<term>Myocytes, Cardiac (metabolism)</term>
<term>Myocytes, Cardiac (ultrastructure)</term>
<term>Proof of Concept Study (MeSH)</term>
<term>Stroke Volume (MeSH)</term>
<term>Ventricular Function, Left (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Antagomirs (administration et posologie)</term>
<term>Aorte (chirurgie)</term>
<term>Aorte (physiopathologie)</term>
<term>Débit systolique (MeSH)</term>
<term>Défaillance cardiaque (génétique)</term>
<term>Défaillance cardiaque (métabolisme)</term>
<term>Défaillance cardiaque (physiopathologie)</term>
<term>Défaillance cardiaque (prévention et contrôle)</term>
<term>Extinction de l'expression des gènes (MeSH)</term>
<term>Fonction ventriculaire gauche (MeSH)</term>
<term>Glutarédoxines (génétique)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Ligature (MeSH)</term>
<term>Mitochondries du myocarde (génétique)</term>
<term>Mitochondries du myocarde (métabolisme)</term>
<term>Mitochondries du myocarde (ultrastructure)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Myocytes cardiaques (métabolisme)</term>
<term>Myocytes cardiaques (ultrastructure)</term>
<term>Mâle (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Souris transgéniques (MeSH)</term>
<term>microARN (génétique)</term>
<term>microARN (métabolisme)</term>
<term>Étude de validation de principe (MeSH)</term>
<term>Études cas-témoins (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antagomirs</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term>
<term>MicroRNAs</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutaredoxins</term>
<term>MicroRNAs</term>
</keywords>
<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Antagomirs</term>
</keywords>
<keywords scheme="MESH" qualifier="chirurgie" xml:lang="fr"><term>Aorte</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Heart Failure</term>
<term>Mitochondria, Heart</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Défaillance cardiaque</term>
<term>Glutarédoxines</term>
<term>Mitochondries du myocarde</term>
<term>microARN</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Heart Failure</term>
<term>Mitochondria, Heart</term>
<term>Myocytes, Cardiac</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Défaillance cardiaque</term>
<term>Glutarédoxines</term>
<term>Mitochondries du myocarde</term>
<term>Myocytes cardiaques</term>
<term>microARN</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Aorte</term>
<term>Défaillance cardiaque</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Aorta</term>
<term>Heart Failure</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Heart Failure</term>
</keywords>
<keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Défaillance cardiaque</term>
</keywords>
<keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Aorta</term>
</keywords>
<keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Mitochondria, Heart</term>
<term>Myocytes, Cardiac</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Case-Control Studies</term>
<term>Disease Models, Animal</term>
<term>Gene Silencing</term>
<term>Humans</term>
<term>Ligation</term>
<term>Male</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Transgenic</term>
<term>Proof of Concept Study</term>
<term>Stroke Volume</term>
<term>Ventricular Function, Left</term>
</keywords>
<keywords scheme="MESH" qualifier="ultrastructure" xml:lang="fr"><term>Animaux</term>
<term>Débit systolique</term>
<term>Extinction de l'expression des gènes</term>
<term>Fonction ventriculaire gauche</term>
<term>Humains</term>
<term>Ligature</term>
<term>Mitochondries du myocarde</term>
<term>Modèles animaux de maladie humaine</term>
<term>Myocytes cardiaques</term>
<term>Mâle</term>
<term>Souris de lignée C57BL</term>
<term>Souris transgéniques</term>
<term>Étude de validation de principe</term>
<term>Études cas-témoins</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>MicroRNAs are small, noncoding RNAs that play a key role in gene expression. Accumulating evidence suggests that aberrant microRNA expression contributes to the heart failure (HF) phenotype; however, the underlying molecular mechanisms are not well understood. A better understanding of the mechanisms of action of microRNAs could potentially lead to targeted therapies that could halt the progression or even reverse HF.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS AND RESULTS</b>
</p>
<p>We found that microRNA-152 (miR-152) expression was upregulated in the failing human heart and experimental animal models of HF. Transgenic mice with cardiomyocyte-specific miR-152 overexpression developed systolic dysfunction (mean difference, -38.74% [95% CI, -45.73% to -31.74%]; </p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>The upregulation of miR-152 expression in the failing myocardium contributes to HF pathophysiology. Preclinical evidence suggests that miR-152 inhibition preserves cardiac function in a model of pressure overload-induced HF. These findings offer new insights into the pathophysiology of HF and point to miR-152-Glrx5 axis as a potential novel therapeutic target.</p>
</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32160771</PMID>
<DateCompleted><Year>2020</Year>
<Month>08</Month>
<Day>17</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>08</Month>
<Day>22</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1941-3297</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>13</Volume>
<Issue>3</Issue>
<PubDate><Year>2020</Year>
<Month>03</Month>
</PubDate>
</JournalIssue>
<Title>Circulation. Heart failure</Title>
<ISOAbbreviation>Circ Heart Fail</ISOAbbreviation>
</Journal>
<ArticleTitle>Pharmacological Silencing of MicroRNA-152 Prevents Pressure Overload-Induced Heart Failure.</ArticleTitle>
<Pagination><MedlinePgn>e006298</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1161/CIRCHEARTFAILURE.119.006298</ELocationID>
<Abstract><AbstractText Label="BACKGROUND">MicroRNAs are small, noncoding RNAs that play a key role in gene expression. Accumulating evidence suggests that aberrant microRNA expression contributes to the heart failure (HF) phenotype; however, the underlying molecular mechanisms are not well understood. A better understanding of the mechanisms of action of microRNAs could potentially lead to targeted therapies that could halt the progression or even reverse HF.</AbstractText>
<AbstractText Label="METHODS AND RESULTS">We found that microRNA-152 (miR-152) expression was upregulated in the failing human heart and experimental animal models of HF. Transgenic mice with cardiomyocyte-specific miR-152 overexpression developed systolic dysfunction (mean difference, -38.74% [95% CI, -45.73% to -31.74%]; <i>P</i>
<0.001) and dilated cardiomyopathy. At the cellular level, miR-152 overexpression perturbed mitochondrial ultrastructure and dysregulated key genes involved in cardiomyocyte metabolism and inflammation. Mechanistically, we identified Glrx5 (glutaredoxin 5), a critical regulator of mitochondrial iron homeostasis and iron-sulfur cluster synthesis, as a direct miR-152 target. Finally, a proof-of-concept of the therapeutic efficacy of targeting miR-152 in vivo was obtained by utilizing a locked nucleic acid-based inhibitor of miR-152 (LNA 152) in a murine model of HF subjected to transverse aortic constriction. We demonstrated that animals treated with LNA-152 (n=10) showed preservation of systolic function when compared with locked nucleic acid-control treated animals (n=9; mean difference, 18.25% [95% CI, 25.10% to 11.39%]; <i>P</i>
<0.001).</AbstractText>
<AbstractText Label="CONCLUSIONS">The upregulation of miR-152 expression in the failing myocardium contributes to HF pathophysiology. Preclinical evidence suggests that miR-152 inhibition preserves cardiac function in a model of pressure overload-induced HF. These findings offer new insights into the pathophysiology of HF and point to miR-152-Glrx5 axis as a potential novel therapeutic target.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>LaRocca</LastName>
<ForeName>Thomas J</ForeName>
<Initials>TJ</Initials>
<AffiliationInfo><Affiliation>Division of Critical Care Medicine, Department of Pediatrics, Lucile Packard Children's Hospital (T.J.L.), Stanford University School of Medicine, CA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Seeger</LastName>
<ForeName>Timon</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Prado</LastName>
<ForeName>Maricela</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Cardiothoracic Surgery (M.P., I.P.-G., I.K.), Stanford University School of Medicine, CA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Perea-Gil</LastName>
<ForeName>Isaac</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Department of Cardiothoracic Surgery (M.P., I.P.-G., I.K.), Stanford University School of Medicine, CA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Neofytou</LastName>
<ForeName>Evgenios</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mecham</LastName>
<ForeName>Brigham H</ForeName>
<Initials>BH</Initials>
<AffiliationInfo><Affiliation>Trialomics, LLC, Seattle, WA (B.H.M.).</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ameen</LastName>
<ForeName>Mohamed</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chang</LastName>
<ForeName>Alex Chia Yu</ForeName>
<Initials>ACY</Initials>
<AffiliationInfo><Affiliation>Department of Cardiology and Shanghai Institute of Precision Medicine, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, China (A.C.Y.C.).</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pandey</LastName>
<ForeName>Gaurav</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Department of Genetics and Genomic Sciences, Icahn Institute of Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY (G.P.).</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Joseph C</ForeName>
<Initials>JC</Initials>
<AffiliationInfo><Affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Radiology (J.C.W.), Stanford University School of Medicine, CA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Karakikes</LastName>
<ForeName>Ioannis</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Department of Cardiothoracic Surgery (M.P., I.P.-G., I.K.), Stanford University School of Medicine, CA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Stanford Cardiovascular Institute (T.S., I.P.-G., E.N., M.A., J.C.W., I.K.), Stanford University School of Medicine, CA.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>K99 HL104002</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R00 HL104002</GrantID>
<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>S10 RR026780</GrantID>
<Acronym>RR</Acronym>
<Agency>NCRR 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>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2020</Year>
<Month>03</Month>
<Day>12</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Circ Heart Fail</MedlineTA>
<NlmUniqueID>101479941</NlmUniqueID>
<ISSNLinking>1941-3289</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000070416">Antagomirs</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C516013">Glrx5 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C550856">MIRN152 microRNA, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D035683">MicroRNAs</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000070416" MajorTopicYN="N">Antagomirs</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001011" MajorTopicYN="N">Aorta</DescriptorName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
<QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020868" MajorTopicYN="Y">Gene Silencing</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006333" MajorTopicYN="N">Heart Failure</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008026" MajorTopicYN="N">Ligation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D035683" MajorTopicYN="N">MicroRNAs</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008929" MajorTopicYN="N">Mitochondria, Heart</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D032383" MajorTopicYN="N">Myocytes, Cardiac</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000075082" MajorTopicYN="N">Proof of Concept Study</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013318" MajorTopicYN="N">Stroke Volume</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016277" MajorTopicYN="N">Ventricular Function, Left</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">heart failure</Keyword>
<Keyword MajorTopicYN="Y">inflammation</Keyword>
<Keyword MajorTopicYN="Y">mice</Keyword>
<Keyword MajorTopicYN="Y">microRNA</Keyword>
<Keyword MajorTopicYN="Y">phenotype</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="pmc-release"><Year>2021</Year>
<Month>03</Month>
<Day>12</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2020</Year>
<Month>3</Month>
<Day>13</Day>
<Hour>6</Hour>
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Pharmacological Silencing of MicroRNA-152 Prevents Pressure Overload-Induced Heart Failure.

Pharmacological Silencing of MicroRNA-152 Prevents Pressure Overload-Induced Heart Failure.

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