ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Targeting Histone Deacetylase 11 with a Highly Selective Inhibitor for the Treatment of MASLD.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- HDAC11 as a potential therapeutic target for Alzheimer's disease.Drug discovery today · 2026Review
- Metabolic dysfunction-associated steatotic liver disease: pathogenesis and novel treatment options.Molecular biomedicine · 2026Review
- Lactate metabolism and lactylation in cancer: from pathogenesis to therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Histone deacetylases: Function in tumor development and therapeutic prospects (Review).Oncology letters · 2026Review
- [Histone deacetylases and alcohol-related liver disease].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin.Journal of experimental & clinical cancer research : CR · 2025Article
- Substrate-Guided Development of HDAC11-Selective Inhibitors Featuring α‑Amino Amide Zinc-Binding Groups.ACS omega · 2025Article
- Recent Insights into the Creation of Histone Deacetylase Inhibitors for the Treatment of Human Diseases.International journal of molecular sciences · 2025Review
- Voriconazole-induced liver injury: incidence patterns and risk factors in a retrospective cohort.Antimicrobial agents and chemotherapy · 2025Article
- Targeting Histone Deacetylase 11 with a Highly Selective Inhibitor for the Treatment of MASLD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) represents the most prevalent chronic liver disorder globally. Due to its intricate pathogenesis and the current lack of efficacious pharmacological interventions, there is a pressing need to discover novel therapeutic targets and agents for MASLD treatment. Herein, it is found that histone deacetylase 11 (HDAC11), a subtype of HDAC family, is markedly overexpressed in both in vitro and in vivo models of MASLD. Furthermore, the knockdown of HDAC11 is observed to mitigate lipid accumulation in hepatic cells. A highly selective HDAC11 inhibitor, B6, which exhibits favorable pharmacokinetic property and liver distribution, is further designed and synthesized. Integrating RNA-seq data with in vivo and in vitro experiments, B6 is found to inhibit de novo lipogenesis (DNL) and promote fatty acid oxidation, thus mitigating hepatic lipid accumulation and pathological symptoms in MASLD mice. Further omics analysis and experiments reveal that B6 enhances the phosphorylation of AMPKα1 at Thr172 through the inhibition of HDAC11, consequently modulating DNL and fatty acid oxidation in the liver. In summary, this study identifies HDAC11 as a potential therapeutic target in MASLD and reports the discovery of a highly selective HDAC11 inhibitor with favorable drug-like properties for the treatment of MASLD.
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