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近年研究表明,细胞凋亡在心肌缺血再灌注损伤(MIRI)中占有重要地位,细胞凋亡与MIRI之间有着密切关系。实验证实他汀类药物具有除调脂以外的心肌保护效应。现主要从他汀类药物的抗氧化作用和激活磷脂酰肌醇-3-激酶丝氨酸-苏氨酸激酶/一氧化氮合酶(PI3K/Akt/eNOS)信号通路两个方面阐述在心肌缺血再灌注过程中他汀类药物抑制心肌细胞凋亡的主要机制。
Recent studies have shown that apoptosis plays an important role in myocardial ischemia-reperfusion injury (MIRI), and there is a close relationship between apoptosis and MIRI. Experiments confirmed that statins have myocardial protection effects other than lipid-lowering. Now mainly from the statin anti-oxidation and activation of phosphatidylinositol 3-kinase serine-threonine kinase / nitric oxide synthase (PI3K / Akt / eNOS) signaling pathways in two aspects of myocardial ischemia again The main mechanism by which statins inhibit cardiomyocyte apoptosis during perfusion.