Section of Cardiology, University of Illinois at Chicago, Chicago, IL 60612, USA.
J Mol Cell Cardiol. 2012 Feb;52(2):454-63. doi: 10.1016/j.yjmcc.2011.09.018. Epub 2011 Sep 25.
Cardiac arrhythmias can cause sudden cardiac death (SCD) and add to the current heart failure (HF) health crisis. Nevertheless, the pathological processes underlying arrhythmias are unclear. Arrhythmic conditions are associated with systemic and cardiac oxidative stress caused by reactive oxygen species (ROS). In excitable cardiac cells, ROS regulate both cellular metabolism and ion homeostasis. Increasing evidence suggests that elevated cellular ROS can cause alterations of the cardiac sodium channel (Na(v)1.5), abnormal Ca(2+) handling, changes of mitochondrial function, and gap junction remodeling, leading to arrhythmogenesis. This review summarizes our knowledge of the mechanisms by which ROS may cause arrhythmias and discusses potential therapeutic strategies to prevent arrhythmias by targeting ROS and its consequences. This article is part of a Special Issue entitled "Local Signaling in Myocytes".
心律失常可导致心源性猝死（SCD），并加剧当前心力衰竭（HF）的健康危机。然而，心律失常的病理过程尚不清楚。心律失常与由活性氧（ROS）引起的系统性和心脏氧化应激有关。在兴奋的心肌细胞中，ROS 调节细胞代谢和离子稳态。越来越多的证据表明，细胞内 ROS 水平升高可导致心脏钠离子通道（Na(v)1.5）改变、Ca(2+)处理异常、线粒体功能变化和缝隙连接重构，从而导致心律失常发生。本文总结了 ROS 引起心律失常的机制，讨论了通过靶向 ROS 及其后果来预防心律失常的潜在治疗策略。本文是题为“心肌细胞内局部信号转导”的特刊的一部分。
