ArticleWorld journal of hepatology2025
ILF3 inhibits p-AMPK expression to drive non-alcoholic fatty liver disease progression.
Article in World journal of hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundNon-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.
aimTo 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
resultsInvestigations 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.
conclusionILF3 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.
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