肝内微环境诱导的自噬在非酒精性脂肪性肝病中的作用
DOI: 10.3969/j.issn.1001-5256.2023.06.029
利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:寇萱萱负责拟定写作思路并撰写文章;张华、邓婧鑫参与相关文献的收集与整理;张建刚审校并修改论文。
Role of intrahepatic microenvironment induced-autophagy in nonalcoholic fatty liver disease
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摘要: 非酒精性脂肪性肝病(NAFLD)是以肝细胞内脂质过度沉积为主要特征的一系列肝脏异常病变,也是全球范围内最常见的慢性肝病。自噬是细胞降解自身成分、参与维持器官功能及机体稳态的一种基本细胞过程,与NAFLD的进展存在密切联系。机体遭受的高脂、缺氧和压力等在肝脏内形成了细胞外微环境的异常改变,这些异常微环境可能通过诱导的肝脏细胞自噬促进NAFLD的发生发展。本文基于肝脏内的多种微环境特征,对肝细胞、Kupffer细胞、肝星状细胞等肝脏细胞的自噬在NAFLD进展中的作用和机制进行综述。Abstract: Nonalcoholic fatty liver disease (NAFLD) is a series of abnormal liver lesions mainly characterized by excessive lipid deposition in hepatocytes, and it is also the most common chronic liver disease worldwide. Autophagy is a basic cellular process in which cells degrade their own components and participate in the maintenance of organ function and body homeostasis, and it is closely associated with the progression of NAFLD. High fat, hypoxia, and stress in human body may cause abnormal changes in extracellular microenvironment in the liver, and such abnormal microenvironment may promote the development and progression of NAFLD by inducing liver cell autophagy. This article reviews the role and mechanism of autophagy of liver cells such as hepatocytes, Kupffer cells, and hepatic stellate cells in the progression of NAFLD based on various microenvironment characteristics in the liver.
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Key words:
- Non-alcoholic Fatty Liver Disease /
- Autophagy /
- Cellular Microenvironment
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