Mitochondria and arrhythmias. Free Radic Biol Med 2014 Jun;71:351-361
Date
04/10/2014Pubmed ID
24713422Pubmed Central ID
PMC4096785DOI
10.1016/j.freeradbiomed.2014.03.033Scopus ID
2-s2.0-84899441965 (requires institutional sign-in at Scopus site) 90 CitationsAbstract
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.
Author List
Yang KC, Bonini MG, Dudley SC JrMESH terms used to index this publication - Major topics in bold
Adenosine TriphosphateAnimals
Antioxidants
Arrhythmias, Cardiac
Calcium
Calcium Channels
Cardiotonic Agents
Humans
Mitochondria, Heart
Myocardium
Myocytes, Cardiac
Oxidation-Reduction
Potassium Channels
Reactive Oxygen Species
Sodium Channels