ILF3 inhibits p-AMPK expression to drive non-alcoholic fatty liver disease progression  

作　　者：Ting Zhan Jia-Xi Liu Min Huang Ming-Tao Chen Xiao-Rong Tian Xiu-Lin Yang Jie Tan Yan-Li Zou Zheng Han Wei Chen Xia Tian Xiao-Dong Huang 

机构地区：[1]Department of Gastroenterology,Wuhan Third Hospital(Tongren Hospital of Wuhan University),Wuhan 430000,Hubei Province,China

出　　处：《World Journal of Hepatology》2025年第2期170-181,共12页世界肝病学杂志(英文)

基　　金：Supported by the Wuhan Science and Technology Bureau Project,No.2022020801020552(to Zhan T);Wuhan Health and Family Planning Commission Medical Research Project,No.WX20M01(to Tian X).

摘　　要：BACKGROUND Non-alcoholic fatty liver disease(NAFLD)is a disease of increasing global prevalence and an important risk factor for the development of insulin resistance,type 2 diabetes,non-alcoholic steatohepatitis and hepatocellular carcinoma,but the pathogenesis is not clear.The aim of this study was to explore the role of ILF3 in NAFLD.AIM To investigate the molecular processes through which ILF3 facilitates the advancement of NAFLD by inhibiting the expression of p-AMPK.This exploration seeks to provide new insights into the etiology of NAFLD and evaluate the potential of ILF3 as a diagnostic marker and potential treatment focus for future interventions.METHODS In vitro and in vivo experiments were conducted using HepG2 cells and NAFLD animal models.The effects of ILF3 knockdown on lipid synthesis and triglyceride(TG)secretion were examined by analyzing the expression levels of p-AMPK.Additionally,the roles of ILF3 and the AMPK signaling pathway were verified using techniques such as Western blotting,quantitative reverse transcription PCR,Oil Red O staining,and immunohistochemistry.RESULTS Investigations revealed an increase in ILF3 Levels within both HepG2 cells and animal models of NAFLD,concurrently with a decrease in p-AMPK expression.Knocking down ILF3 activated the AMPK pathway,reducing lipid production and TG secretion in hepatocytes,thereby mitigating the advancement of NAFLD.CONCLUSION ILF3 promotes the evolution of NAFLD by inhibiting the expression of p-AMPK.The knockdown of ILF3 activates the AMPK signaling pathway,alleviating the severity of NAFLD.These findings underscore the function of ILF3 in the pathogenesis of NAFLD and demonstrate its viability as a treatment focus and diagnostic indicator.

关 键 词：Non-alcoholic fatty liver disease ILF3 AMPK pathway Lipid metabolism Therapeutic target Molecular mechanism 

分 类 号：R575.5[医药卫生—消化系统]