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

Fadi G. Akar

Research output: Contribution to journalReview articlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)249-258
Number of pages10
JournalJournal of Interventional Cardiac Electrophysiology
Issue number3
StatePublished - Sep 2013


  • Arrhythmia
  • Hypertrophy
  • Ischemia-reperfusion injury
  • Mitochondria
  • Oxidative stress
  • Reactive oxygen species

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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