Journal
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
Volume 52, Issue 2, Pages 454-463Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2011.09.018
Keywords
Reactive oxygen species; Sodium channel; Ca2+ handling; Mitochondria; Connexin; Arrhythmia
Categories
Funding
- National Institutes of Health [R01 HL085558, R01 HL073753, P01 HL058000]
- Veterans Affairs MERIT
- American Heart Association [AHA10POST4450037]
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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 Ca2+ 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. (C) 2011 Elsevier Ltd. All rights reserved.
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