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Mitochondrial Damage in Myocardial Ischemia/Reperfusion Injury and Application of Natural Plant Products.
Su, Xin; Zhou, Mingyang; Li, Yingjian; An, Na; Yang, Fan; Zhang, Guoxia; Xu, Lianjiang; Chen, Hengwen; Wu, Hongjin; Xing, Yanwei.
Affiliation
  • Su X; Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Zhou M; Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
  • Li Y; Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
  • An N; Beijing University of Chinese Medicine, Beijing, China.
  • Yang F; Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Zhang G; Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Xu L; Hebei Gangkou Hospital, Qinhuangdao, Hebei, China.
  • Chen H; Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Wu H; Boao International Hospital, Shanghai University of Traditional Chinese Medicine, Qionghai, China.
  • Xing Y; Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Oxid Med Cell Longev ; 2022: 8726564, 2022.
Article in En | MEDLINE | ID: mdl-35615579
ABSTRACT
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.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Biological Products / Myocardial Reperfusion Injury / Myocardial Ischemia Limits: Humans Language: En Journal: Oxid Med Cell Longev Journal subject: METABOLISMO Year: 2022 Document type: Article Affiliation country:

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Biological Products / Myocardial Reperfusion Injury / Myocardial Ischemia Limits: Humans Language: En Journal: Oxid Med Cell Longev Journal subject: METABOLISMO Year: 2022 Document type: Article Affiliation country: