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Role of Mitochondria in Nonalcoholic Fatty Liver Disease

机译:线粒体在非酒精性脂肪肝疾病中的作用

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Nonalcoholic fatty liver disease (NAFLD) affects about 30% of the general population in the United States and includes a spectrum of disease that includes simple steatosis, non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis. Significant insight has been gained into our understanding of the pathogenesis of NALFD; however the key metabolic aberrations underlying lipid accumulation in hepatocytes and the progression of NAFLD remain to be elucidated. Accumulating and emerging evidence indicate that hepatic mitochondria play a critical role in the development and pathogenesis of steatosis and NAFLD. Here, we review studies that document a link between the pathogenesis of NAFLD and hepatic mitochondrial dysfunction with particular focus on new insights into the role of impaired fatty acid oxidation, the transcription factor peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), and sirtuins in development and progression of NAFLD.
机译:非酒精性脂肪肝疾病(NAFLD)影响美国约30%的普通人群,包括一系列疾病,包括单纯性脂肪变性,非酒精性脂肪性肝炎(NASH),纤维化和肝硬化。我们对NALFD的发病机理有了深入的了解。然而,尚需阐明肝细胞脂质蓄积和NAFLD进展的关键代谢异常。越来越多的证据表明,肝线粒体在脂肪变性和NAFLD的发生和发病中起着关键作用。在这里,我们回顾研究,这些研究记录了NAFLD的发病机理与肝线粒体功能障碍之间的联系,特别着重于对受损的脂肪酸氧化的作用,转录因子过氧化物酶体增殖物激活的受体-γcoactivator-1α(PGC-1α ),以及在NAFLD发生和发展中的沉默调节蛋白。

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