Enhanced NCLX-dependent mitochondrial Ca²⁺ efflux attenuates pathological remodeling in heart failure.

ABSTRACT: Mitochondrial calcium (_mCa²⁺) uptake couples changes in cardiomyocyte energetic demand to mitochondrial ATP production. However, excessive _mCa²⁺ uptake triggers permeability transition and necrosis. Despite these established roles during acute stress, the involvement of _mCa²⁺ signaling in cardiac adaptations to chronic stress remains poorly defined. Changes in NCLX expression are reported in heart failure (HF) patients and models of cardiac hypertrophy. Therefore, we hypothesized that altered _mCa²⁺ homeostasis contributes to the hypertrophic remodeling of the myocardium that occurs upon a sustained increase in cardiac workload. The impact of _mCa²⁺ flux on cardiac function and remod

SUBMITTER: Garbincius JF 

PROVIDER: S-EPMC9107512 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature