Mitochondrial Ca²⁺, redox environment and ROS emission in heart failure: Two sides of the same coin?

ABSTRACT: Heart failure (HF) is a progressive, debilitating condition characterized, in part, by altered ionic equilibria, increased ROS production and impaired cellular energy metabolism, contributing to variable profiles of systolic and diastolic dysfunction with significant functional limitations and risk of premature death. We summarize current knowledge concerning changes of intracellular Na⁺ and Ca²⁺ control mechanisms during the disease progression and their consequences on mitochondrial Ca²⁺ homeostasis and the shift in redox balance. Absent existing biological data, our computational modeling studies advance a new 'in silico' analysis to reconcile existing opposing views, based on different experimental HF models, regarding variations in mitochondrial Ca

SUBMITTER: Cortassa S 

PROVIDER: S-EPMC7880885 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature