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线粒体作为细胞存活和死亡的主宰者发挥多种功能作用,包括氧化-磷酸化作用、自由基生成以及维持细胞内Ca2+平衡。在心肌缺血过程中以及缺血后,线粒体Ca2+浓度升高、功能受损,最终导致细胞坏死或凋亡。本文主要从线粒体Ca2+浓度升高出现的原因、对线粒体功能的病理性调控作用及其诱导的自身保护机制几个方面,综述了Ca2+在心肌缺血/再灌注损伤的线粒体调控机制中的作用。
Mitochondria play a number of functional roles as masters of cell survival and death, including oxidative-phosphorylation, free radical generation and maintenance of intracellular Ca2 + balance. During myocardial ischemia and after ischemia, the concentration of mitochondrial Ca2 + is elevated and impaired in function, eventually leading to cell necrosis or apoptosis. This article mainly reviews the role of Ca2 + in the mitochondrial regulatory mechanism of myocardial ischemia / reperfusion injury from the aspects of mitochondrial Ca2 + concentration rise, pathological regulation of mitochondrial function and its self-protection mechanism.