自噬
脂肪肝
脂肪性肝炎
脂肪变性
酒精性肝病
肝损伤
内科学
肝病
酒精性脂肪肝
脂滴
发病机制
疾病
生物
医学
癌症研究
肝硬化
线粒体
细胞生物学
细胞凋亡
生物化学
作者
Bilon Khambu,Shengmin Yan,Nazmul Huda,Gang Liu,Xiao‐Ming Yin
出处
期刊:Liver Research
[Elsevier]
日期:2018-09-01
卷期号:2 (3): 112-119
被引量:76
标识
DOI:10.1016/j.livres.2018.09.004
摘要
Autophagy is an evolutionarily conserved intracellular degradative function that is important for liver homeostasis. Accumulating evidence suggests that autophagy is deregulated during the progression and development of alcoholic and non-alcoholic liver diseases. Impaired autophagy prevents the clearance of excessive lipid droplets (LDs), damaged mitochondria, and toxic protein aggregates, which can be generated during the progression of various liver diseases, thus contributing to the development of steatosis, injury, steatohepatitis, fibrosis, and tumors. In this review, we look at the status of hepatic autophagy during the pathogenesis of alcoholic and non-alcoholic liver diseases. We also examine the mechanisms of defects in autophagy, and the hepato-protective roles of autophagy in non-alcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD), focusing mainly on steatosis and liver injury. Finally, we discuss the therapeutic potential of autophagy modulating agents for the treatment of these two common liver diseases.
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