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Tranilast inhibits hepatic lipid response in nonalcoholic steatohepatitis by deacetylating LKB1

GSE249350 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2025/02/19 Platform GPL24247
Summary
Nonalcoholic fatty liver disease (NAFLD), a progressive hepatic disease with ectopic fat accumulation, can evolve toward nonalcoholic steatohepatitis (NASH). To date, there is still no approved drug therapy, which remains a major unmet need. Previous study has indicated that tranilast ameliorates hepatic fibrosis and stellate cells activation in dietary rat model of NASH. However, the precise mechanism of tranilast in anti-NASH remains unclear.
Published in
Small molecule-driven LKB1 deacetylation is responsible for the inhibition of hepatic lipid response in NAFLD
Qin W, Ding Y, Zhang W et al. · Journal of lipid research 2025 · PMID 39755206 · doi:10.1016/j.jlr.2024.100740
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Also filed as BioProject PRJNA1048840 and SRA study SRP475914. Searching any of these in the dataset finder brings you back here.

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