Mitochondrial reactive oxygen species and atrial fibrillation |
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| Authors: | ZHENG An-cai LI Ju-xiang |
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| Institution: | Department of Cardiology, The Second Affiliated Hospital, Nanchang University, Nanchang 330006, China |
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| Abstract: | Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. Mitochondrial oxidative stress is supposed to contribute to development, progression and self-perpetuation of AF. Reactive oxygen species (ROS) is the major molecule mediating mitochondrial oxidative stress damage. ROS can alter the redox status of various molecular targets, which quite specifically leads to functional alterations of ion channel activity or activation of a variety of redox sensitive signal transduction pathways. Eventually, it leads to atrial electrical remodeling and promotes the development of AF. Therefore, mitochondrial oxidative stress pathways may be a new target for the therapy of atrial fibrillation. |
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| Keywords: | Mitochondrial Reactive oxygen species Ion channel Atrial fibrillation |
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