脂肪性肝炎
脂肪肝
肝硬化
脂肪变性
纤维化
酒精性肝病
信号转导
慢性肝病
生物
医学
生物信息学
疾病
内科学
细胞生物学
作者
Chengyuan Liang,Juan Li,Bin Tian,Lei Tian,Yuzhi Liu,Jingyi Li,Liang Xin,Jun Wang,Chao Fu,Zhenfeng Shi,Juan Xia,Yiting Liang,Kun Wang
标识
DOI:10.1016/j.biopha.2021.112298
摘要
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, and it is a liver manifestation of metabolic syndrome, with a histological spectrum from simple steatosis to non-alcoholic steatohepatitis (NASH). NASH can evolve into progressive liver fibrosis and eventually lead to liver cirrhosis. The pathological mechanism of NASH is multifactorial, involving a series of metabolic disorders and changes that trigger low-level inflammation in the liver and other organs. In the pathogenesis of NASH, the signal transduction pathway involving succinate and the succinate receptor (G-protein-coupled receptor 91, GPR91) regulates inflammatory cell activation and liver fibrosis. This review describes the mechanism of the succinate-GPR91 signalling pathway in NASH and summarizes the drugs that act on this pathway, with the aim of providing a new approach to NASH treatment.
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