Mitochondria and arrhythmias

Kai Chien Yang, Marcelo G. Bonini, Samuel C. Dudley*

*Corresponding author for this work

Research output: Contribution to journalReview article

45 Scopus citations

Abstract

Mitochondria are essential to providing ATP, thereby satisfying the energy demand of the incessant electrical activity and contractile action of cardiac muscle. Emerging evidence indicates that mitochondrial dysfunction can adversely affect cardiac electrical functioning by impairing the intracellular ion homeostasis and membrane excitability through reduced ATP production and excessive reactive oxygen species (ROS) generation, resulting in increased propensity to cardiac arrhythmias. In this review, the molecular mechanisms linking mitochondrial dysfunction to cardiac arrhythmias are discussed with an emphasis on the impact of increased mitochondrial ROS on the cardiac ion channels and transporters that are critical to maintaining normal electromechanical functioning of the cardiomyocytes. The potential of using mitochondria-targeted antioxidants as a novel antiarrhythmia therapy is highlighted.

Original languageEnglish (US)
Pages (from-to)351-361
Number of pages11
JournalFree Radical Biology and Medicine
Volume71
DOIs
StatePublished - Jun 2014

Keywords

  • Calcium
  • Free radicals
  • Heart
  • Ion channels
  • Reactive oxygen species
  • Sudden death

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)

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