Metabolic stress, reactive oxygen species, and arrhythmia

Euy Myoung Jeong, Man Liu, Megan Sturdy, Ge Gao, Susan T. Varghese, Ali A. Sovari, Samuel C. Dudley

Research output: Contribution to journalReview articlepeer-review

158 Scopus citations


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 v1.5), 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".

Original languageEnglish (US)
Pages (from-to)454-463
Number of pages10
JournalJournal of Molecular and Cellular Cardiology
Issue number2
StatePublished - Feb 2012
Externally publishedYes

Bibliographical note

Funding Information:
This study was funded by National Institutes of Health grants, R01 HL085558, R01 HL073753, P01 HL058000 , and a Veterans Affairs MERIT grant (SCD). Dr. Sovari received an American Heart Association Midwest Affiliate Postdoctoral Fellowship #AHA10POST4450037.


  • Arrhythmia
  • Ca handling
  • Connexin
  • Mitochondria
  • Reactive oxygen species
  • Sodium channel


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