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 sensi -tive 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 .

作者：郑安财；李菊香

来源：中国病理生理杂志 2017 年 33卷 10期