Abstract
Stress-induced Ca2+-dependent arrhythmias have been attributed to the increased propensity of ventricular myocytes (VMs) to diastolic Ca2+ waves (DCWs), secondary to mitochondria-dependent oxidation of ryanodine receptors (RyRs), sarcoplasmic reticulum (SR) Ca2+-release channels. We have recently shown that RyR-mediated Ca2+ release regulates mitochondrial reactive oxygen species (ROS) production. Mito-ROS production is affected by organization degree of Electron Transport Chain (ETC) components into quaternary supercomplexes.
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