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

ABSTRACT: Altered levels of intracellular calcium (Ca²⁺) 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 Ca²⁺ 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 Ca²⁺-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 m

SUBMITTER: Eberhardt DR 

PROVIDER: S-EPMC9107497 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature