Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 71, Issue -, Pages 351-361Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2014.03.033
Keywords
Reactive oxygen species; Ion channels; Sudden death; Heart; Calcium; Free radicals
Funding
- National Institutes of Health [RO1 HL104025, HL106592]
- Veterans Affairs MERIT Grant [BX000859]
- American Heart Association [AHA13POST14380029, 13GRNT16400010, 09SDG2250933]
- U.S. Department of Defense [W911NF-12-1-0493]
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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. (C) 2014 Elsevier Inc. All rights reserved.
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