EFHD1 ablation inhibits cardiac mitoflash activation and protects cardiomyocytes from ischemia.

Autor: Eberhardt DR; Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), University of Utah, United States of America., Lee SH; Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), University of Utah, United States of America., Yin X; Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), University of Utah, United States of America., Balynas AM; Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), University of Utah, United States of America., Rekate EC; Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), University of Utah, United States of America., Kraiss JN; Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), University of Utah, United States of America., Lang MJ; Diabetes & Metabolism Research Center, University of Utah, United States of America., Walsh MA; Diabetes & Metabolism Research Center, University of Utah, United States of America., Streiff ME; Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), University of Utah, United States of America; Department of Biomedical Engineering, University of Utah, United States of America., Corbin AC; Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), University of Utah, United States of America; Department of Biomedical Engineering, University of Utah, United States of America., Li Y; Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, United States of America., Funai K; Diabetes & Metabolism Research Center, University of Utah, United States of America., Sachse FB; Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), University of Utah, United States of America; Department of Biomedical Engineering, University of Utah, United States of America., Chaudhuri D; Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), University of Utah, United States of America; Department of Biomedical Engineering, University of Utah, United States of America; Department of Internal Medicine, Division of Cardiovascular Medicine, University of Utah, Salt Lake City, UT, United States of America. Electronic address: dipayan.chaudhuri@hsc.utah.edu.
Jazyk: angličtina
Zdroj: Journal of molecular and cellular cardiology [J Mol Cell Cardiol] 2022 Jun; Vol. 167, pp. 1-14. Date of Electronic Publication: 2022 Mar 16.
DOI: 10.1016/j.yjmcc.2022.03.002
Abstrakt: Altered levels of intracellular calcium (Ca 2+ ) are a highly prevalent feature in different forms of cardiac injury, producing changes in contractility, arrhythmias, and mitochondrial dysfunction. In cardiac ischemia-reperfusion injury, mitochondrial Ca 2+ overload leads to pathological production of reactive oxygen species (ROS), activates the permeability transition, and cardiomyocyte death. Here we investigated the cardiac phenotype caused by deletion of EF-hand domain-containing protein D1 (Efhd1 -/- ), a Ca 2+ -binding mitochondrial protein whose function is poorly understood. Efhd1 -/- mice are viable and have no adverse cardiac phenotypes. They feature reductions in basal ROS levels and mitoflash events, both important precursors for mitochondrial injury, though cardiac mitochondria have normal susceptibility to Ca 2+ overload. Notably, we also find that Efhd1 -/- mice and their cardiomyocytes are resistant to hypoxic injury.
(Copyright © 2022 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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