Mitochondrial Damage in Myocardial Ischemia/Reperfusion Injury and Application of Natural Plant Products

被引:18
作者
Su, Xin [1 ]
Zhou, Mingyang [2 ]
Li, Yingjian [2 ]
An, Na [3 ]
Yang, Fan [1 ]
Zhang, Guoxia [1 ]
Xu, Lianjiang [4 ]
Chen, Hengwen [1 ]
Wu, Hongjin [5 ]
Xing, Yanwei [1 ]
机构
[1] China Acad Chinese Med Sci, Guanganmen Hosp, Beijing, Peoples R China
[2] Capital Med Univ, Beijing Anzhen Hosp, Beijing, Peoples R China
[3] Beijing Univ Chinese Med, Beijing, Peoples R China
[4] Hebei Gangkou Hosp, Qinhuangdao, Hebei, Peoples R China
[5] Shanghai Univ Tradit Chinese Med, Boao Int Hosp, Qionghai, Peoples R China
基金
国家重点研发计划; 中国国家自然科学基金;
关键词
ISCHEMIA-REPERFUSION INJURY; PERMEABILITY TRANSITION PORE; OXIDATIVE STRESS; ESSENTIAL COMPONENT; THERAPEUTIC TARGET; INFARCT SIZE; I/R INJURY; CELL-DEATH; RAT HEARTS; CALCIUM;
D O I
10.1155/2022/8726564
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Ischemic heart disease (IHD) is currently one of the leading causes of death among cardiovascular diseases worldwide. In addition, blood reflow and reperfusion paradoxically also lead to further death of cardiomyocytes and increase the infarct size. Multiple evidences indicated that mitochondrial function and structural disorders were the basic driving force of IHD. We summed up the latest evidence of the basic associations and underlying mechanisms of mitochondrial damage in the event of ischemia/reperfusion (I/R) injury. This review then reviewed natural plant products (NPPs) which have been demonstrated to mitochondria-targeted therapeutic effects during I/R injury and the potential pathways involved. We realized that NPPs mainly maintained the integrality of mitochondria membrane and ameliorated dysfunction, such as improving abnormal mitochondrial calcium handling and inhibiting oxidative stress, so as to protect cardiomyocytes during I/R injury. This information will improve our knowledge of mitochondrial biology and I/R-induced injury's pathogenesis and exhibit that NPPs hold promise for translation into potential therapies that target mitochondria.
引用
收藏
页数:19
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