Small molecule-driven LKB1 deacetylation is responsible for the inhibition of hepatic lipid response in NAFLD.

ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is a progressive condition characterized by ectopic fat accumulation in the liver, for which no FAD-approved drugs currently exist. Emerging evidence highlights the role of liver kinase B1 (LKB1), a key metabolic regulator, has been proposed in NAFLD, particularly in response to excessive nutrient levels. However, few agents have been identified that can prevent the progression of nonalcoholic steatohepatitis (NASH) by targeting LKB1 deacetylation. Through comprehensive screening of our in-house chemical library, we identified tranilast, a small molecule with remarkable inhibitory efficacy against lipid deposition induced by palmitic acid/oleic acid (PO). In this study, we investigated the novel biological function and mechanism of tranilast in regu

SUBMITTER: Qin W 

PROVIDER: S-EPMC11808498 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature