Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan.
Center for Mitochondrial Research and Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan.
Cells. 2020 Apr 22;9(4):1041. doi: 10.3390/cells9041041.
Non-alcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease and ranges from steatosis to steatohepatitis and to liver fibrosis. Lipotoxicity in hepatocytes, elevated oxidative stress and the activation of proinflammatory mediators of Kupffer cells, and fibrogenic pathways of activated hepatic stellate cells can contribute to the development of NAFLD. MicroRNAs (miRs) play a crucial role in the dysregulated metabolism and inflammatory signaling connected with NAFLD and its progression towards more severe stages. Of note, the protective effect of non-coding miR-29a on liver damage and its versatile action on epigenetic activity, mitochondrial homeostasis and immunomodulation may improve our perception of the pathogenesis of NAFLD. Herein, we review the biological functions of critical miRs in NAFLD, as well as highlight the emerging role of miR-29a in therapeutic application and the recent advances in molecular mechanisms underlying its liver protective effect.
非酒精性脂肪性肝病（NAFLD）是一种常见的慢性肝病，其范围从脂肪变性到脂肪性肝炎再到肝纤维化。肝细胞中的脂毒性、氧化应激的升高以及库普弗细胞中促炎介质的激活，以及活化的肝星状细胞的纤维生成途径都可能导致 NAFLD 的发生。微小 RNA（miRs）在与 NAFLD 及其向更严重阶段进展相关的代谢失调和炎症信号转导中起着至关重要的作用。值得注意的是，非编码 miR-29a 对肝损伤的保护作用及其对表观遗传活性、线粒体动态平衡和免疫调节的多效作用可能会改善我们对 NAFLD 发病机制的认识。本文综述了关键 miR 在 NAFLD 中的生物学功能，并强调了 miR-29a 在治疗应用中的新兴作用及其在肝保护作用的分子机制方面的最新进展。
