ArticleInternational journal of biological sciences2025
Pharmacological Activation of AMP-activated Protein Kinase Ameliorates Liver Fibrosis in a Metabolic Dysfunction-Associated Steatohepatitis Mouse Model.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Sanzi Sijun Formula Alleviates Lipotoxic Liver Injury in Metabolic Dysfunction-Associated Steatotic Liver Disease via AMPK/SIRT1 Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Trilobatin is associated with reduced lipid accumulation in multiple biological models: insights from transcriptomics, molecular docking, and molecular dynamics simulations.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Comparative analysis of renal dysfunction, immune remodeling, and gut microbiota profiles in dietary models of metabolic liver disease.BMC nephrology · 2026Article
- Crosstalk along the gut-liver axis modulates glutathione and cadmium-induced hepatotoxicity.Frontiers in immunology · 2026Review
- Molecular and cellular mechanisms of pentadecanoic acid.World journal of biological chemistry · 2025Review
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Authors and funding
10 authors.
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Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) is a significant contributor to hepatocellular carcinoma (HCC). To validate AMPK activation as a therapeutic strategy for MASH-associated liver fibrosis, we investigated the effects of a 4-chloro-benzenesulfonamide derivative named KN21, a novel AMPK activator, on the liver fibrogenic process in a MASH model. In mice fed a choline-deficient, L-amino acid-defined, high fat diet (CDAHFD), KN21 reduced hepatic steatosis, lipid accumulation, and liver fibrosis. In hepatocyte cells treated with palmitic acid and oleic acid (PO), KN21 attenuated lipid accumulation and the release of reactive oxygen species (ROS) and fibrotic mediators. Hepatic stellate cells stimulated with hepatocyte-derived conditioned medium (CM) exhibited increased expression of fibrosis markers, whereas hepatic stellate cells exposed to CM from KN21-treated hepatocytes showed a decrease of fibrosis marker expression. Additionally, KN21 inhibited the activation of human hepatic stellate cells and demonstrated potent antifibrotic activity. These findings underscore the therapeutic potential of pharmacological AMPK activation for the treatment of MASH-associated liver fibrosis.
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