Yang Kai-Chien, Bonini Marcelo G, Dudley Samuel C
Lifespan Cardiovascular Institute, Providence VA Medical Center, and Brown University, Providence, RI 02903, USA.
Department of Medicine/Cardiology, University of Illinois at Chicago, Chicago, IL 60612, USA; Department of Pathology, and University of Illinois at Chicago, Chicago, IL 60612, USA; Department of Pharmacology, University of Illinois at Chicago, Chicago, IL 60612, USA.
Free Radic Biol Med. 2014 Jun;71:351-361. doi: 10.1016/j.freeradbiomed.2014.03.033. Epub 2014 Apr 5.
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.
线粒体对于提供三磷酸腺苷（ATP）至关重要，从而满足心肌持续电活动和收缩作用的能量需求。新出现的证据表明，线粒体功能障碍可通过减少ATP生成和过度产生活性氧（ROS）损害细胞内离子稳态和膜兴奋性，进而对心脏电功能产生不利影响，导致心律失常的倾向增加。在本综述中，我们讨论了将线粒体功能障碍与心律失常联系起来的分子机制，重点是线粒体ROS增加对心脏离子通道和转运体的影响，这些离子通道和转运体对于维持心肌细胞正常的机电功能至关重要。本文还强调了使用线粒体靶向抗氧化剂作为一种新型抗心律失常疗法的潜力。
