自噬
脂肪肝
肝星状细胞
细胞生物学
酒精性肝病
癌症研究
纤维化
脂滴
脂毒性
疾病
生物
平衡
肝病
医学
病理
肝硬化
内科学
内分泌学
细胞凋亡
生物化学
糖尿病
胰岛素抵抗
作者
Qi Shen,Ming Yang,Li Wang,Yukui Zhang,S N Chen,Jingliang Zhang,Zhuang Xiong,Qingsen Ran
标识
DOI:10.3389/fendo.2024.1374644
摘要
Non-alcoholic fatty liver disease (NAFLD) is a clinicopathologic syndrome characterized by excessive fat deposition in hepatocytes and a major cause of end-stage liver disease. Autophagy is a metabolic pathway responsible for degrading cytoplasmic products and damaged organelles, playing a pivotal role in maintaining the homeostasis and functionality of hepatocytes. Recent studies have shown that pharmacological intervention to activate or restore autophagy provides benefits for liver function recovery by promoting the clearance of lipid droplets (LDs) in hepatocytes, decreasing the production of pro-inflammatory factors, and inhibiting activated hepatic stellate cells (HSCs), thus improving liver fibrosis and slowing down the progression of NAFLD. This article summarizes the physiological process of autophagy, elucidates the close relationship between NAFLD and autophagy, and discusses the effects of drugs on autophagy and signaling pathways from the perspectives of hepatocytes, kupffer cells (KCs), and HSCs to provide assistance in the clinical management of NAFLD.
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