ArticleJournal of translational medicine2025
Treg and intestinal myofibroblasts-derived Amphiregulin induced by TGF-β mediates intestinal fibrosis in Crohn's disease.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The trial behind it
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
12 citing papers in PubMed.
- Tropomyosin-1 positively regulates TGF-β/Smad3 signaling through STUB1 in arecoline-induced oral submucosal fibrosis.Odontology · 2026Article
- Review
- Regulatory T cells in cancer and inflammation.Signal transduction and targeted therapy · 2026Review
- An intricate relationship between fibrosis and autoimmune diseases: a specific focus on unraveling its molecular, immunological, and epigenetic drivers.Frontiers in immunology · 2026Review
- Multimodal biomarkers and prediction models for stricturing and penetrating progression in Crohn's disease.Frontiers in medicine · 2026Review
- Striking a balance: how the gut microbiome shapes the fate of intestinal CD4+ T cells.Discovery immunology · 2026Review
- From Polymorphisms to Phenotypes:Genes · 2025Article
- Recent Updates on Molecular and Physical Therapies for Organ Fibrosis.Molecules (Basel, Switzerland) · 2025Review
- Amphiregulin and Fibrosis: Existing Evidence and Future Directions.International journal of molecular sciences · 2025Review
- Aging and Intestinal Fibrosis: Mechanisms, Implications, and Therapeutic Strategies.Clinical interventions in aging · 2025Review
- Immunological mechanisms underlying fibrotic diseases via single-cell technologies.Frontiers in immunology · 2025Review
- The emerging role of tissue regulatory T cells in tissue repair and regeneration.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
backgroundIntestinal fibrosis is a serious complication of Crohn's disease (CD), often resulting from chronic inflammation. However, the precise mechanisms through which inflammation induces intestinal fibrosis remain inadequately elucidated.
methodsA comprehensive single-cell atlas of full-thickness CD, provided by Dr. Florian Rieder, was subjected to reanalysis. Our study used a DSS-induced chronic colitis model in both wild-type (WT) and Areg
resultsSeveral types of cells were differentially expressed between stricture and non-stricture CD. Among T cells, Tregs accounted for a larger proportion and were significantly increased in stenotic tissues of stricture CD. Although DSS-induced colitis was more severe in Areg
conclusionThese findings demonstrated that AREG derived from Tregs and human intestinal MFs, induced by TGF-β, amplifies intestinal fibrotic reactions in experimental colitis as well as in human CD patients. Thus, the TGF-β-Smad3-AREG pathway could be a potential therapeutic target for treating fibrosis in CD.
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Registered trials
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