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在急性心肌梗死时,过量产生的活性氧和细胞内钙积聚对启动程序性细胞死亡起重要作用。细胞死亡包括坏死、凋亡、自噬及其共同作用。在缺血过程中,肌浆网、肌丝之间的钙处理被中断,同时钙转移至线粒体导致其肿胀,再灌注激活能量传导和心肌收缩导致氧自由基释放及其他离子失衡,在急性缺血-再灌注过程中,主要的死亡途径是线粒体通透性转换孔开放和线粒体外膜通透性增加启动内源性程序性坏死和凋亡。尽管国内外学者做了深入的研究,但调节线粒体膜通透性的作用和机制尚未完全了解。外源性凋亡、坏死性凋亡和自噬也可能加重缺血-再灌注所致的损伤。在这篇综述中,我们将讨论心肌梗死时钙失调和氧自由基、Bcl-2蛋白、线粒体膜通透性改变在心肌细胞死亡途径中的作用。
In acute myocardial infarction, excessive production of reactive oxygen species and intracellular calcium accumulation plays an important role in the initiation of programmed cell death. Cell death includes necrosis, apoptosis, autophagy and their synergy. In the process of ischemia, calcium treatment between sarcoplasmic reticulum and myofilament is interrupted, and calcium is transferred to the mitochondria to cause swelling. Reperfusion energy transfer and myocardial contractions lead to the release of oxygen free radicals and other ion imbalances. In acute deficiencies, During the blood-reperfusion process, the main pathways of death are the opening of mitochondrial permeability transition pore and the increase of mitochondrial outer membrane permeability to initiate endogenous programmed necrosis and apoptosis. Although domestic and foreign scholars have done in-depth research, the role and mechanism of regulating mitochondrial membrane permeability have not yet been fully understood. Exogenous apoptosis, necrotic apoptosis and autophagy may also aggravate ischemia-reperfusion injury. In this review, we will discuss the role of calcium imbalance and oxygen free radicals, Bcl-2 protein, and mitochondrial membrane permeability changes in cardiomyocyte death pathway during myocardial infarction.