ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2024
FXR deletion attenuates intestinal barrier dysfunction in murine acute intestinal inflammation.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The gut microbiome-bile acid-FXR interplay: a pivotal axis in metabolic and gastrointestinal diseases.Gut microbes · 2026Review
- Bile salt hydrolase activity as a rational target for MASLD therapy.Gut microbes · 2026Article
- Bariatric and metabolic surgery improves glycolipid metabolism via bile acid regulation and intestinal barrier repair in T2DM patients.Journal of medical biochemistry · 2026Article
- Mechanisms and therapeutic prospects of DNA methylation-mucosal innate immunity crosstalk in inflammatory bowel disease.Frontiers in immunology · 2026Review
- Review: microbial metabolites - a key to address gut inflammation and barrier dysfunction in the premature infant.Gut microbes · 2025Review
- Advances of exosome regulating‑FXR to repair inflammatory bowel disease (Review).International journal of molecular medicine · 2025Review
- Bile acids affect intestinal barrier function through FXR and TGR5.Frontiers in medicine · 2025Review
- Bile Acids in Inflammatory Bowel Disease: From Pathophysiology to Treatment.Biomedicines · 2024Review
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Funding
Abstract
Accumulating literature suggests that the farnesoid-X receptor (FXR), a nuclear bile acid receptor best known for its role in bile acid homeostasis, is also a potent context-dependent regulator of inflammation. FXR may thus be relevant to several intestinal disease states including inflammatory bowel disease, necrotizing enterocolitis, and sepsis. In this study, we tested the effects of FXR deletion on acute murine intestinal inflammation. We found that FXR knockout (KO) mice were protected from intestinal injury and barrier dysfunction induced by lipopolysaccharide (LPS) injection, dithizone (DI)/
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