ReviewInflammatory intestinal diseases2023
Molecular Basis of Intestinal Fibrosis in Inflammatory Bowel Disease.
Review in Inflammatory intestinal diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 25 citations in OpenAlex.
- Intestinal Fibrosis in IBD: Rethinking the Inflammatory Paradigm and Emerging Therapeutic Opportunities.Digestive diseases and sciences · 2026Review
- Prior vedolizumab exposure and fibroblast-derived MMP13 are associated with ustekinumab nonresponse in ulcerative colitis.Journal of gastroenterology · 2026Article
- Article
- Optimized air-liquid interface cultivation enhances survival and integrity of mouse colon precision-cut tissue slices.Scientific reports · 2026Article
- Advancing IBD Management: A Literature Review on the Role of Non-Invasive Blood-Based Biomarkers in Predicting and Assessing Pharmacodynamic Response to Treatment.Clinical and translational science · 2026Review
- Analysis of Periostin, TGF-β, and SLUG Expression in Inflammatory Bowel Disease in Pediatric Patients and Their Clinical Implications.Journal of clinical medicine · 2026Article
- Treat-to-Target in Ulcerative Colitis: How Soon Is Now?Journal of clinical medicine · 2026Article
- Baseline stool TIMP-2 predicts strictures and penetrating disease progression in Crohn's patients.Frontiers in immunology · 2026Article
- Beyond inflammation: what drives the self-perpetuating cycle of fibrosis in IBD?Annals of medicine · 2025Review
- DCLK1 isoform (DCLK1-S) as a critical player in promoting inflammation, tissue remodeling, and EMT in mouse models of colitis.PLoS pathogens · 2025Article
- Molecular Basis of Chronic Intestinal Wall Fibrosis in Inflammatory Bowel Diseases.International journal of molecular sciences · 2025Review
- Disease-Specific Novel Role of Growth Differentiation Factor 15 in Organ Fibrosis.International journal of molecular sciences · 2025Review
- Intestinal Fibrosis in Crohn's Disease: Pathophysiology, Diagnosis, and New Therapeutic Targets.Journal of clinical medicine · 2025Review
- Chronic Gastrointestinal Disorders and miRNA-Associated Disease: An Up-to-Date.International journal of molecular sciences · 2025Review
- Cannabidiol Alleviates Intestinal Fibrosis in Mice with Ulcerative Colitis by Regulating Transforming Growth Factor Signaling Pathway.Journal of inflammation research · 2025Article
- Phytochemical Compounds as Promising Therapeutics for Intestinal Fibrosis in Inflammatory Bowel Disease: A Critical Review.Nutrients · 2024Review
- Inhibition of intestinal inflammation and fibrosis by Scutellaria Baicalensis georgi and Boswellia serrata in human epithelial cells and fibroblasts.Immunity, inflammation and disease · 2024Article
- 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
- Fisetin modulates the gut microbiota alongside biomarkers of senescence and inflammation in a DSS-induced murine model of colitis.GeroScience · 2024Article
- TL1A Promotes Fibrogenesis in Colonic Fibroblasts via the TGF-β1/Smad3 Signaling Pathway.Current medical science · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Intestinal fibrosis in Crohn's disease (CD) is considered to be irreversible and induces persistent luminal narrowing and strictures. In the past decades, substantial advances have been made in the understanding of the cellular and molecular mechanisms underlying intestinal fibrosis in inflammatory bowel disease (IBD). Summary: Intestinal fibrosis is typically associated with mesenchymal cell hyperplasia, tissue disorganization, and deposition of extracellular matrix (ECM). The transient appearance of mesenchymal cells is a feature of normal wound healing, but the persistence of these cells is associated with ECM deposition and fibrosis, leading to loss of normal architecture and function. When homeostatic control of the repair process becomes dysregulated, perpetual activation of profibrotic responses and sustained accumulation of ECM are induced. In the process of intestinal fibrosis, myofibroblasts are considered to be the key effector cells, being responsible for the synthesis of ECM proteins. Activation and accumulation of myofibroblasts in the stricturing lesions of CD patients are mediated by various factors such as growth factors, cytokines, epithelial-to-mesenchymal or endothelial-to-mesenchymal transitions. Despite the identification of many putative targets and target pathways applicable to antifibrotic therapies, no such treatment has yet been successful. Predictive biomarkers and non-invasive diagnostic tools for intestinal fibrosis are still insufficient in IBD. Key Message: We summarize recent advances in the understanding of the cellular and molecular mechanisms underlying intestinal fibrosis in IBD.
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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.