未折叠蛋白反应
蛋白质稳态
内质网
脂肪肝
脂肪性肝炎
脂肪变性
炎症体
医学
细胞生物学
酒精性肝病
癌症研究
胰岛素抵抗
内科学
生物
炎症
疾病
胰岛素
肝硬化
作者
Cynthia Lebeaupin,Déborah Vallée,Younis Hazari,Claudio Hetz,Éric Chevet,Béatrice Bailly-Maître
标识
DOI:10.1016/j.jhep.2018.06.008
摘要
The global epidemic of obesity has been accompanied by a rising burden of non-alcoholic fatty liver disease (NAFLD), with manifestations ranging from simple steatosis to non-alcoholic steatohepatitis, potentially developing into hepatocellular carcinoma. Although much attention has focused on NAFLD, its pathogenesis remains largely obscure. The hallmark of NAFLD is the hepatic accumulation of lipids, which subsequently leads to cellular stress and hepatic injury, eventually resulting in chronic liver disease. Abnormal lipid accumulation often coincides with insulin resistance in steatotic livers and is associated with perturbed endoplasmic reticulum (ER) proteostasis in hepatocytes. In response to chronic ER stress, an adaptive signalling pathway known as the unfolded protein response is triggered to restore ER proteostasis. However, the unfolded protein response can cause inflammation, inflammasome activation and, in the case of non-resolvable ER stress, the death of hepatocytes. Experimental data suggest that the unfolded protein response influences hepatic tumour development, aggressiveness and response to treatment, offering novel therapeutic avenues. Herein, we provide an overview of the evidence linking ER stress to NAFLD and discuss possible points of intervention.
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