Mitochondrial targets for arrhythmia suppression: is there a role for pharmacological intervention?

Abstract

Mitochondrial dysfunction is a hallmark of common cardiovascular disorders, including ischemia-reperfusion injury, hypertrophy, heart failure, and diabetes mellitus. While the role of the mitochondrial network in regulating energy production and cell death pathways is well established, its active control of other critical cellular functions, including excitation-contraction coupling and excitability, is less understood. The purpose of this focused review article is to highlight the growing mechanistic link between mitochondrial dysfunction and arrhythmogenesis. The goal is not to provide a comprehensive listing of all factors by which mitochondrial bioenergetics and altered cellular redox status affect ion channel function but rather to focus on one central mechanism of arrhythmogenesis which arises from a mitochondrial origin. In doing so, we discuss the role of mitochondrial targets for suppressing arrhythmias through this mechanism.