Mitochondrial reactive oxygen species and atrial fibrillation
10.3969/j.issn.1000-4718.2017.10.031
- VernacularTitle:线粒体ROS与心房颤动
- Author:
cai An ZHENG
1
;
xiang Ju LI
Author Information
1. 南昌大学第二附属医院心内科,江西南昌330006
- Keywords:
Mitochondrial;
Reactive oxygen species;
Ion channel;
Atrial fibrillation
- From:
Chinese Journal of Pathophysiology
2017;33(10):1917-1920
- CountryChina
- Language:Chinese
-
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 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 .
