MCU overexpression evokes disparate dose-dependent effects on mito-ROS and spontaneous Ca²⁺ release in hypertrophic rat cardiomyocytes.

ABSTRACT: Cardiac dysfunction in heart failure (HF) and diabetic cardiomyopathy (DCM) is associated with aberrant intracellular Ca²⁺ handling and impaired mitochondrial function accompanied with reduced mitochondrial calcium concentration (mito-[Ca²⁺]). Pharmacological or genetic facilitation of mito-Ca²⁺ uptake was shown to restore Ca²⁺ transient amplitude in DCM and HF, improving contractility. However, recent reports suggest that pharmacological enhancement of mito-Ca²⁺ uptake can exacerbate ryanodine receptor-mediated spontaneous sarcoplasmic reticulum (SR) Ca²⁺ release in ventricular myocytes (VMs) from diseased animals, increasing propensity to stress-induced ventricular tachyarrhythmia. To test whether chronic recovery of mito-

SUBMITTER: Hamilton S 

PROVIDER: S-EPMC8794228 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature