ArticleNature communications2014
PPARα-UGT axis activation represses intestinal FXR-FGF15 feedback signalling and exacerbates experimental colitis.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.
- Fermented Dairy Food Intake and Risk of Colorectal Cancer: A Systematic Review and Meta-Analysis.Frontiers in oncology · 2022Pooled it
- Microbial 10-oxostearic acid protects mice against colitis via the nuclear receptor PPARα.Nature microbiology · 2026Article
- Chenodeoxycholic acid redirects the bile acid synthetic pathway to limit pro-inflammatory neutrophil infiltration and alleviate colitis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- The role of bile acid dynamics in inflammatory bowel disease and metabolic dysfunction-associated steatotic liver disease.Liver research (Beijing, China) · 2026Review
- Organ cross-talk: molecular mechanisms, biological functions, and therapeutic interventions for diseases.Signal transduction and targeted therapy · 2026Review
- Multiomics Reveals Nonphagocytosable Microplastics Induce Colon Inflammatory Injury via Bile Acid-Gut Microbiota Interactions and Barrier Dysfunction.ACS applied materials & interfaces · 2025Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Inhibition of Farnesoid-x-receptor signaling during abdominal sepsis by dysbiosis exacerbates gut barrier dysfunction.Cell communication and signaling : CCS · 2025Article
- Sedanolide alleviates DSS-induced colitis by modulating the intestinal FXR-SMPD3 pathway in mice.Journal of advanced research · 2025Article
- Microbiota governs host chenodeoxycholic acid glucuronidation to ameliorate bile acid disorder induced diarrhea.Microbiome · 2025Article
- Reversing metabolic dysregulation in farnesoid X receptor knockout mice via gut microbiota modulation.PloS one · 2025Article
- Changes in Serum Bilirubin and Total Bile Acids During Biologic Therapy in Patients with Ulcerative Colitis: A Retrospective Study.Journal of inflammation research · 2025Article
- Phillygenin ameliorates tight junction proteins reduction, fibrosis, and apoptosis in mice with chronic colitis via TGR5-mediated PERK-eIF2α-CaJournal of pharmaceutical analysis · 2025Article
- How bile acids and the microbiota interact to shape host immunity.Nature reviews. Immunology · 2024Review
- Bile Acid Signaling in Metabolic and Inflammatory Diseases and Drug Development.Pharmacological reviews · 2024Review
- Article
- Cucurbitacin IIb alleviates colitis via regulating gut microbial composition and metabolites.Heliyon · 2024Article
- Article
- Bile acids and coronavirus disease 2019.Acta pharmaceutica Sinica. B · 2024Review
- Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Bile acids play a pivotal role in the pathological development of inflammatory bowel disease (IBD). However, the mechanism of bile acid dysregulation in IBD remains unanswered. Here we show that intestinal peroxisome proliferator-activated receptor α (PPARα)-UDP-glucuronosyltransferases (UGTs) signalling is an important determinant of bile acid homeostasis. Dextran sulphate sodium (DSS)-induced colitis leads to accumulation of bile acids in inflamed colon tissues via activation of the intestinal peroxisome PPARα-UGTs pathway. UGTs accelerate the metabolic elimination of bile acids, and thereby decrease their intracellular levels in the small intestine. Reduced intracellular bile acids results in repressed farnesoid X receptor (FXR)-FGF15 signalling, leading to upregulation of hepatic CYP7A1, thus promoting the de novo bile acid synthesis. Both knockout of PPARα and treatment with recombinant FGF19 markedly attenuate DSS-induced colitis. Thus, we propose that intestinal PPARα-UGTs and downstream FXR-FGF15 signalling play vital roles in control of bile acid homeostasis and the pathological development of colitis.
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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.