Mitochondrial Damage in Myocardial Ischemia/Reperfusion Injury and Application of Natural Plant Products.
Xin SuMingyang ZhouYingjian LiNa AnFan YangGuoxia ZhangLianjiang XuHengwen ChenHongjin WuYanwei XingPublished in: Oxidative medicine and cellular longevity (2022)
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.
Keyphrases
- oxidative stress
- ischemia reperfusion injury
- diabetic rats
- dna damage
- induced apoptosis
- cell death
- cardiovascular disease
- high glucose
- acute myocardial infarction
- healthcare
- endoplasmic reticulum
- signaling pathway
- heart failure
- type diabetes
- brain injury
- cerebral ischemia
- human health
- drug delivery
- health information
- heat shock
- blood brain barrier
- single molecule
- climate change
- cardiovascular risk factors
- metabolic syndrome
- social media
- endoplasmic reticulum stress
- acute ischemic stroke
- heat shock protein