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非酒精性脂肪性肝病(non-alcoholic fatty liver disease,NAFLD)包括肝细胞脂肪变性(Hepatic Stestosis)、非酒精性脂肪性肝炎(non-alcoholic steatohepatitis,NASH)以及由此而引起的肝纤维化和肝硬化(Cirrhosis),更有个别在此基础上发展为肝细胞癌(Hepatocellular Carcinoma,HCC)。近年来随着生活水平的改善和生活方式的改变,NAFLD的发病率不断升高,但其病因和发病机制尚未完全明了。肝细胞凋亡和半胱天冬蛋白酶系统(Caspase)的激活可能导致了肝脏损伤和NAFLD的进展。线粒体膜通透性转换孔(mitochondrial permeability transition pore,MPTP)是线粒体内外信息交流的中心枢纽,其开放状态可以导致线粒体跨膜电位(ΔΨm)毁减、细胞色素C(Cytochrome-C,Cyt-C)和凋亡诱导因子(apoptosis-inducing factor,AIF)释放到胞浆,从而决定着线粒体功能的发挥并诱导细胞凋亡的发生。因此探讨MPTP与NAFLD的关系对研究NAFLD的发病机制具有重要意义。本文综述了MPTP在非酒精性脂肪肝发病中的作用。
Non-alcoholic fatty liver disease (NAFLD) includes Hepatic Stestosis, non-alcoholic steatohepatitis (NASH) and the resulting liver fibrosis and Cirrhosis, on the other hand, develops hepatocellular carcinoma (HCC) on its own. In recent years, with the improvement of living standards and lifestyle changes, the incidence of NAFLD continues to rise, but its etiology and pathogenesis are not yet fully understood. Hepatocyte apoptosis and activation of the caspase system may lead to liver damage and progression of NAFLD. Mitochondrial membrane permeability transition pore (MPTP) is the central hub of information exchange inside and outside mitochondria. Its open state can lead to the destruction of mitochondrial transmembrane potential (ΔΨm), cytochrome C (Cyt-C, Cyt-C ) And apoptosis-inducing factor (AIF) release to the cytoplasm, which determines the mitochondrial function and induce the occurrence of apoptosis. Therefore, to explore the relationship between MPTP and NAFLD is of great significance for studying the pathogenesis of NAFLD. This article reviews the role of MPTP in the pathogenesis of non-alcoholic fatty liver disease.