Research progress on mechanism of traditional Chinese medicine in improving myocardial ischemia-reperfusion injury by mitochondrial quality control
- VernacularTitle:中药通过线粒体质量控制改善心肌缺血再灌注损伤的机制研究进展
- Author:
Gaojing ZHANG
1
,
2
;
Zhiyu YUAN
2
;
Xincan LIU
1
,
2
;
Tianfu SUN
1
,
2
;
Zhenzhen LAN
1
Author Information
1. Cardiac Center，the First Affiliated Hospital of Henan University of Chinese Medicine，Zhengzhou 450099，China
2. Dept. of Cardiology，the First Affiliated Hospital of Henan University of Chinese Medicine，Zhengzhou 450099，China
- Publication Type:Journal Article
- Keywords:
traditional Chinese medicine;
myocardial ischemia-reperfusion injury;
mitochondrial quality control
- From:
China Pharmacy
2025;36(12):1542-1546
- CountryChina
- Language:Chinese
-
Abstract:
Myocardial ischemia-reperfusion injury （MIRI） is a common cardiac pathological process， resulting from the combined effects of multiple mechanisms involving metabolic changes and mitochondrial dysfunction. Mitochondrial quality control （MQC）， as a key regulatory mechanism， may serve as an important target for the prevention and treatment of MIRI. In recent years， traditional Chinese medicine （TCM） has demonstrated unique advantages in the field of improving MIRI， with multiple targets， multiple pathways， and low toxic and side effects. It has gained widespread clinical recognition and application. Through systematically organizing and summarizing recent studies on the targeting of MQC by monomers， active fractions， herb pairs， compound formulas and related preparations of TCM to improve MIRI， this paper finds that monomers and active fractions of TCM （such as schisandrin B， isoliquiritigenin， calenduloside E， berberine， Lycium barbarum polysaccharides and so on） as well as TCM herb pairs， compound formulas， and related preparations （couplet medicinals of Fuzi-Ganjiang， Yixin formula， Shuangshen ningxin capsule， Baijin formula， Yiqi huoxue decoction and so on）， can alleviate MIRI by activating MQC to reduce oxidative stress-induced damage， promote mitochondrial biogenesis， maintain mitochondrial fission/fusion homeostasis， regulate mitochondrial autophagy， and restore mitochondrial calcium homeostasis.
