Ganoderic acid A alleviates metabolic dysfunction-associated fatty liver disease through attenuating steatosis and cellular apoptosis by targeting acetyl-CoA carboxylase.

Authors

Yang Yao, Zhujun Liu, Xujiao Wang, Cunhao Bian, Na Yin, Xiaoyu Peng, Siqian Qin, Rui Wang, Yukun Zhang

Published in

International immunopharmacology. Volume 186. Pages 117108. Jul 04, 2026. Epub Jul 04, 2026.

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a global metabolic epidemic with no specific effective therapy, characterized by hepatic steatosis and excessive hepatocyte apoptosis. This study explored the protective effects and mechanisms of Ganoderic acid A (GA-A) against MASLD. In high-fat diet (HFD)-fed mice and palmitic acid (PA)-stimulated HepG2 cells, GA-A notably relieved hepatic steatosis, liver injury, lipid metabolic disorders and hepatocyte apoptosis. Acetyl-CoA carboxylase (ACC) was identified as a direct target of GA-A via protein microarray, molecular docking, SPR, CETSA and Co-IP assays. Mechanistically, GA-A activated the AMPK-ACC pathway and suppressed ACC activity. Application of the ACC inhibitor ND646 and ACC silencing partially abrogated GA-A's therapeutic effects, confirming both ACC-dependent and independent actions. Collectively, GA-A directly targets ACC to ameliorate MASLD, indicating its potential as a promising candidate drug for this metabolic liver disease.

PMID:
42401090
Bibliographic data and abstract were imported from PubMed on 05 Jul 2026.

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