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线粒体是急性缺血/再灌注损伤后决定心肌细胞命运的重要细胞器。再灌注初期线粒体通透性转换孔(mitochondrial permeability transition pore,MPTP)开放可介导细胞死亡。应用药物抑制剂(如环孢素A)或基因手段抑制再灌注初期MPTP开放可减少急性心肌缺血/再灌注损伤后的心肌梗死面积,且缺血处理的内源性心肌保护作用机制中也包含MPTP开放抑制。MPTP抑制剂环孢素A在治疗心肌缺血/再灌注损伤方面有一定效果,但由于其特异性较低,新的特异性更高的MPTP抑制剂有待被研发。本文就MPTP在心肌急性缺血/再灌注损伤及其相关干预性保护措施中作用的研究进展作一综述。
Mitochondria are important organelles that determine the fate of cardiomyocytes after acute ischemia / reperfusion injury. Mitochondrial permeability transition pore (MPTP) opening during early reperfusion can mediate cell death. Inhibition of MPTP opening during early reperfusion with a drug inhibitor (such as cyclosporin A) or gene therapy reduces myocardial infarct size after acute myocardial ischemia / reperfusion injury, and endogenous myocardial protective mechanisms of ischemic treatment Contains MPTP open inhibitory. The MPTP inhibitor cyclosporin A has some effect in the treatment of myocardial ischemia / reperfusion injury, but due to its low specificity, a new and more specific MPTP inhibitor has yet to be developed. This article reviews the research progress of the role of MPTP in acute myocardial ischemia / reperfusion injury and its related protective measures.