Metabolic Stress, Reactive Oxygen Species, and Arrhythmia
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Date
2012-02Author
Jeong, Euy-Myoung
Liu, Man
Sturdy, Megan
Gao, Ge
Sovari, Ali A.
Dudley, Samuel C.
Publisher
ElsevierMetadata
Show full item recordAbstract
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.
Subject
reactive oxygen speciessodium channel
arrhythmia
connexin
mitochondria