Metabolic stress, reactive oxygen species, and arrhythmia

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".

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Anti-Arrhythmia Agents / pharmacology
  • Anti-Arrhythmia Agents / therapeutic use
  • Arrhythmias, Cardiac / drug therapy
  • Arrhythmias, Cardiac / metabolism*
  • Calcium / metabolism
  • Humans
  • Mitochondria, Heart / drug effects
  • Mitochondria, Heart / metabolism
  • Oxidation-Reduction / drug effects
  • Oxidative Stress / physiology*
  • Potassium Channels / metabolism
  • Reactive Oxygen Species / metabolism*


  • Anti-Arrhythmia Agents
  • Potassium Channels
  • Reactive Oxygen Species
  • Calcium