Restricting mitochondrial GRK2 post-ischemia confers cardioprotection by reducing myocyte death and maintaining glucose oxidation-Reference-Cited by-同舟云学术

Restricting mitochondrial GRK2 post-ischemia confers cardioprotection by reducing myocyte death and maintaining glucose oxidation

Published:2018-12-11 Issue:560 Volume:11 Page:
ISSN:1945-0877
Container-title:Science Signaling
language:en
Short-container-title:Sci. Signal.

Author:

Sato Priscila Y.¹²³^ORCID,Chuprun J. Kurt¹²,Grisanti Laurel A.¹²⁴,Woodall Meryl C.¹²,Brown Brett R.¹²^ORCID,Roy Rajika¹²^ORCID,Traynham Christopher J.¹²,Ibetti Jessica¹²^ORCID,Lucchese Anna M.¹²^ORCID,Yuan Ancai¹²,Drosatos Konstantinos¹²^ORCID,Tilley Doug G.¹²,Gao Erhe¹²,Koch Walter J.¹²^ORCID

Affiliation:

1. Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.

2. Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.

3. Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.

4. Department of Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia, MO 65211, USA.

Abstract

Preventing GRK2 from localizing to mitochondria lessens the damage induced by myocardial infarction.

Funder

National Institutes of Health

W.W. Smith Charitable Trust

American Heart Association

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference43 articles.

1. The Evolving Impact of G Protein-Coupled Receptor Kinases in Cardiac Health and Disease

2. Inhibition of G-protein-coupled Receptor Kinase 2 (GRK2) Triggers the Growth-promoting Mitogen-activated Protein Kinase (MAPK) Pathway

3. Level of G protein–Coupled Receptor Kinase-2 Determines Myocardial Ischemia/Reperfusion Injury via Pro- and Anti-Apoptotic Mechanisms

4. Cardiac G-Protein–Coupled Receptor Kinase 2 Ablation Induces a Novel Ca 2+ Handling Phenotype Resistant to Adverse Alterations and Remodeling After Myocardial Infarction

5. Prodeath Signaling of G Protein–Coupled Receptor Kinase 2 in Cardiac Myocytes After Ischemic Stress Occurs Via Extracellular Signal–Regulated Kinase-Dependent Heat Shock Protein 90–Mediated Mitochondrial Targeting

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