ArticleJournal of advanced research2026
Senkyunolide A interrupts TRAF6-HDAC3 interaction to epigenetically suppress c-MYC and attenuate cholestatic liver injury.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- LncRNA H19 as a key regulator in biliary atresia: insights into pathogenesis and potential therapeutic targets.Annals of medicine · 2026Review
- Long non-coding RNA antisense of insulin-like growth factor 2 receptor promotes osteogenic differentiation by enhancing runt-related transcription factor 2 translation: A potential therapeutic target for osteoporosis.Journal of advanced research · 2026Article
- Wireless flexible patch based on ultrasound-responsive SenA@ZIF-8 release for on-demand medication of periodontitis.Journal of nanobiotechnology · 2026Article
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Authors and funding
14 authors.
Funding
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Abstract
Introduction Cholestatic liver diseases are highly prevalent and lack effective treatment, ultimately progressing to end-stage liver diseases. Our recent study indicates that the interplay between c-MYC and lncRNA H19 exacerbates the ductular reaction during cholestasis.
objectiveThis study aims to unveil the underlying mechanisms of the protective effects of senkyunolide A (SenA) on cholangiocyte overproliferation in cholestatic liver diseases.
methodsThrough comprehensive characterization using RNA sequencing, CHIP analysis, protein truncation, amino acid mutation or deletion, and the development of SenA derivatives, we explored the effects and mechanisms of SenA in vivo in bile duct ligation mice and in vitro in primary cholangiocytes.
resultsWe demonstrated that SenA effectively mitigates cholangiocyte hyperproliferation by epigenetically suppressing c-MYC expression and disrupting the downstream H19, Let-7a and Lin28a. Mechanically, we identified a potential interaction between the carbonyl group in SenA and Arg483 in TRAF6, disrupting the TRAF6-HDAC3 complex. This dissociation facilitates the binding of HDAC3 to the MYC promoter region, resulting in enhanced histone deacetylation and transcriptional suppression.
conclusionWe highlight the therapeutic potential of SenA in cholestatic liver diseases by elucidating its role in epigenetic regulation.
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