ArticleMedComm2025
Disruption of Bile Acid Metabolism in the Gut-Liver Axis Predisposes Mice to Inflammatory Bowel Disease.
Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Hydrogel-Based Therapeutic Strategies for Post-Cholecystectomy NAFLD: Targeting Bile Acid Signaling, Gut Microbiota, Inflammation, and Hepatic Fibrosis.Gels (Basel, Switzerland) · 2026Review
- Graft bile analysis for predicting post-transplant outcomes: A literature review and a protocol for a novel biomarker.World journal of gastrointestinal surgery · 2026Review
- Polysaccharides from the root tubers ofFrontiers in pharmacology · 2026Article
- Therapeutic modulation of the gut microbiota by traditional Chinese medicine in the management of cholestatic liver injury.Frontiers in cellular and infection microbiology · 2026Review
- Disruption of Bile Acid Metabolism in the Gut-Liver Axis Predisposes Mice to Inflammatory Bowel Disease.MedComm · 2025Article
- TCDCA inhibits pyroptosis to alleviate sepsis-related acute hepatic injury via activating TGR5.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease that is frequently associated with inflammatory bowel disease (IBD). However, the precise mechanisms linking these conditions remain unclear. In this study, we established a murine model of experimental sclerosing cholangitis (eSC) using a DDC (3,5-diethoxycarbonyl 1,4-dihydrocollidine) diet. We then demonstrated that eSC mice exhibited increased susceptibility to DSS-induced colitis, accompanied by severe intestinal pathology. Further integrated analyses revealed that eSC disrupted bile acid metabolism and gut microbiota composition, notably increasing Th17-inducing bacteria and altering bile acid profiles. Single-cell and bulk RNA-seq analyses identified a marked expansion of colonic Th17 cells and a loss of immune homeostasis in eSC mice. Therapeutically, rectal administration of lithocholic acid (LCA) and its derivative, 3-Oxo-5β-cholanoic acid (3-O-LCA), was found to restore farnesoid X receptor (FXR) signaling, reduce Th17 cell proportions, and alleviate liver and intestinal injury. Mechanistic studies show that LCA and 3-O-LCA modulate macrophage polarization and Th17 differentiation via FXR. These findings highlight the central role of the gut-liver axis, bile acid signaling, and Th17 responses in PSC-IBD pathogenesis, and suggest that targeting bile acid metabolism offers a promising therapeutic strategy. This work advances our understanding of PSC-IBD and provides a foundation for novel interventions in high-risk patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.