ArticleMediators of inflammation2021
Effect and Mechanism of TL1A Expression on Epithelial-Mesenchymal Transition during Chronic Colitis-Related Intestinal Fibrosis.
Article in Mediators of inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- TL1A as a therapeutic renaissance in inflammatory bowel disease: a systematic review from molecular mechanisms to clinical translation.Journal of Crohn's & colitis · 2026Pooled it
- Acupuncture and Moxibustion Inhibited Intestinal Epithelial-Mesenchymal Transition in Patients with Crohn's Disease Induced by TGF- β 1/Smad3/Snail Pathway: A Clinical Trial Study.Chinese journal of integrative medicine · 2022Trial
- Intestinal Fibrosis in IBD: Rethinking the Inflammatory Paradigm and Emerging Therapeutic Opportunities.Digestive diseases and sciences · 2026Review
- Mast cell-derived IL-13 as a driver of Crohn disease-associated intestinal fibrosis.Inflammatory bowel diseases · 2026Article
- Treat-to-Target in Ulcerative Colitis: How Soon Is Now?Journal of clinical medicine · 2026Article
- GB20-5A8-31, an anti-TL1A antibody for treating inflammatory bowel disease.Frontiers in immunology · 2026Article
- The Therapeutic Potential of Targeting TL1A in a Spectrum of Inflammatory Disorders.Journal of inflammation research · 2026Review
- Developments in the connection between epithelial‑mesenchymal transition and endoplasmic reticulum stress (Review).International journal of molecular medicine · 2025Review
- Intestinal Fibrosis in Crohn's Disease: Pathophysiology, Diagnosis, and New Therapeutic Targets.Journal of clinical medicine · 2025Review
- TL1A as a Target in Inflammatory Bowel Disease: Exploring Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2025Review
- TL1A Inhibition in Inflammatory Bowel Disease: A Pipeline Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025Review
- Type 2 immunity in allergic diseases.Cellular & molecular immunology · 2025Review
- Inflammation-fibrosis interplay in inflammatory bowel disease: mechanisms, progression, and therapeutic strategies.Frontiers in pharmacology · 2025Review
- Characterization of patient-derived intestinal organoids for modelling fibrosis in Inflammatory Bowel Disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Inflammation accelerating intestinal fibrosis: from mechanism to clinic.European journal of medical research · 2024Review
- TL1A Promotes Fibrogenesis in Colonic Fibroblasts via the TGF-β1/Smad3 Signaling Pathway.Current medical science · 2024Article
- Epigenetic Regulation of EMP/EMT-Dependent Fibrosis.International journal of molecular sciences · 2024Review
- Article
- Antibodies Targeting the Tumor Necrosis Factor-Like Ligand 1A in Inflammatory Bowel Disease: A New Kid on the (Biologics) Block?Digestion · 2024Review
- Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsRecent evidences reveal that epithelial to mesenchymal transition (EMT) exacerbates the process of intestinal fibrosis. Tumor necrosis factor-like ligand 1A (TL1A) is a member of the tumor necrosis family (TNF), which can take part in the development of colonic inflammation and fibrosis by regulating immune response or inflammatory factors. The purpose of this study was to elucidate the possible contribution of TL1A in onset and progression of intestinal inflammation and fibrosis through EMT.
methodsColonic specimens were obtained from patients with inflammatory bowel disease (IBD) and control individuals. The expression levels of TL1A and EMT-related markers in intestinal tissues were evaluated. Furthermore, the human colorectal adenocarcinoma cell line, HT-29, was stimulated with TL1A, anti-TL1A antibody, or BMP-7 to assess EMT process. In addition, transgenic mice expressing high levels of TL1A in lymphoid cells were used to further investigate the mechanism of TL1A in intestinal fibrosis.
resultsHigh levels of TL1A expression were detected in the intestinal specimens of patients with ulcerative colitis and Crohn's disease and were negatively associated with the expression of an epithelial marker (E-cadherin), while it was positively associated with the expression of interstitial markers (FSP1 and
conclusionsTL1A participates in the formation and process of EMT in intestinal fibrosis. This new knowledge enables us to better understand the pathogenesis of intestinal fibrosis and identify new therapeutic targets for its treatment.
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Registered trials
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