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    Metabolic Stress, Reactive Oxygen Species, and Arrhythmia

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    JMCC 6003 resubmission.pdf (379.6Kb)
    Date
    2012-02
    Author
    Jeong, Euy-Myoung
    Liu, Man
    Sturdy, Megan
    Gao, Ge
    Sovari, Ali A.
    Dudley, Samuel C.
    Publisher
    Elsevier
    Metadata
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    Abstract
    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 species
    sodium channel
    arrhythmia
    connexin
    mitochondria
    Type
    Article
    Date available in INDIGO
    2012-06-27T21:55:57Z
    URI
    http://hdl.handle.net/10027/8397
    Collections
    • Publications - Cardiology

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