Mitochondria and arrhythmias

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

Research output: Contribution to journalReview articlepeer-review

48 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
Externally publishedYes

Bibliographical note

Funding Information:
This work was funded by National Institutes of Health Grants RO1 HL104025 (S.C.D.) and HL106592 (S.C.D.), Veterans Affairs MERIT Grant BX000859 (S.C.D.), and American Heart Association Midwest Affiliation Postdoctoral Fellowship AHA13POST14380029 (K.C.Y.); Dr. Bonini is funded by the American Heart Association ( 13GRNT16400010 ; 09SDG2250933 ) and the U.S. Department of Defense W911NF-12-1-0493 ). Dr. Dudley is an inventor of 13/551,790 “A Method for Ameliorating or Preventing Arrhythmic Risk Associated with Cardiomyopathy by Improving Conduction Velocity” and 13/507,319 “A Method for Modulating or Controlling Connexin43 (Cx43) Level of a Cell and Reducing Arrhythmic Risk.”

Keywords

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

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