ReviewInflammatory bowel diseases2014
Mechanisms that mediate the development of fibrosis in patients with Crohn's disease.
Review in Inflammatory bowel diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
What it found
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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
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Management of ileocolic anastomotic strictures in Crohn's disease: endoscopic or surgical intervention? A systematic review and meta-analysis.International journal of colorectal disease · 2025Pooled it
- Multi-Omics and Machine Learning-Based Characterization of the Lactylation Microenvironment and Biomarker Identification in Crohn's Disease Intestinal Fibrosis.International journal of molecular sciences · 2026Article
- Mechanostimulatory Cues Determine Intestinal Fibroblast Fate and Profibrotic Remodeling in a Physiodynamic Human Gut-on-a-Chip.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Deciphering immune and cellular reprogramming during the progression from inflammatory bowel disease to colorectal cancer using multi-omics single-cell and spatial transcriptomics.Journal of translational medicine · 2026Article
- Generative AI-augmented transcriptomic and microbiome analysis across inflammatory and fibrotic disease states in Crohn's disease.Frontiers in artificial intelligence · 2026Article
- Ustekinumab enhances intestinal stenosis resolution by modulating fibrotic pathways in crohn's disease: a retrospective single-center study with translational analysis.BMC gastroenterology · 2025Article
- Spatiotemporal analysis of Crohn's disease reveals PECAM2 signaling at the basis of the inflammation-to-fibrosis transition.Journal of Crohn's & colitis · 2025Article
- Targeting the double-edged sword: cytokines in the pathogenesis and treatment of autoimmune diseases.Inflammopharmacology · 2025Review
- Molecular Basis of Chronic Intestinal Wall Fibrosis in Inflammatory Bowel Diseases.International journal of molecular sciences · 2025Review
- Intestinal Fibrosis in Crohn's Disease: Pathophysiology, Diagnosis, and New Therapeutic Targets.Journal of clinical medicine · 2025Review
- Quantitative Magnetic Resonance Imaging (qMRI) of the Small Bowel in Crohn's Disease: State-of-the-Art and Future Directions.Journal of magnetic resonance imaging : JMRI · 2025Review
- SAA3 deficiency exacerbates intestinal fibrosis in DSS-induced IBD mouse model.Cell death discovery · 2025Article
- Macrophage Metabolic Reprogramming in Inflammatory Bowel Diseases: From Pathogenesis to Therapy.Journal of inflammation research · 2025Review
- Protease-activated Receptor 2 Promotes Crohn's Disease-Associated Colonic Fibrosis through Fibroblast Activation.Current molecular medicine · 2025Article
- The role of molecular imaging in detecting fibrosis in Crohn's disease.Annals of medicine · 2024Review
- The Impact of Pentraxin 3 on Crohn's Disease Phenotype.International journal of molecular sciences · 2024Article
- Quantitative MRI in children with Crohn's disease - where do we stand?Pediatric radiology · 2024Review
- The transcription factor HIF-1α in NKp46+ ILCs limits chronic intestinal inflammation and fibrosis.Life science alliance · 2024Article
- Fibrostenosing Crohn's Disease: Pathogenetic Mechanisms and New Therapeutic Horizons.International journal of molecular sciences · 2024Review
- Challenges in IBD Research 2024: Preclinical Human IBD Mechanisms.Inflammatory bowel diseases · 2024Review
5 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
2 authors at 1 institution in 2 countries.
Funding
Abstract
Crohn's disease is complicated by the development of fibrosis and stricture in approximately 30% to 50% of patients over time. The pathogenesis of fibrostenotic disease is multifactorial involving the activation of mesenchymal cells by cytokines, growth factors, and other mediators released by immune cells, epithelial cells, and mesenchymal cells. Transforming growth factor β, a key activator of mesenchymal cells, is central to the process of fibrosis and regulates numerous genes involved in the disordered wound healing including collagens, and other extracellular matrix proteins, connective tissue growth factor, and insulin-like growth factors. The activated mesenchymal compartment is expanded by recruitment of new mesenchymal cells through epithelial to mesenchymal transition, endothelial to mesenchymal transition, and invasion of circulating fibrocytes. Cellular hyperplasia and increased extracellular matrix production, particularly collagens, from fibroblasts, myofibroblasts, and smooth muscle cells add to the disturbed architecture and scarring on the intestine. Extracellular matrix homeostasis is further disrupted by alterations in the expression of matrix metalloproteinases and tissue inhibitors of metalloproteinase in the gut. Among the 163 susceptibility genes identified that contribute to susceptibility in inflammatory bowel disease mutations in NOD2/CARD15, innate immune system components and autophagy jointly contribute to the activation of mesenchymal cells and pathogenesis of fibrosis in this polygenic disorder. Numerous growth factors cytokines and other mediators also contribute to development of fibrosis in the susceptible patient. This review focuses on the molecular mechanisms that regulate mesenchymal cell function, particularly smooth muscle cells, the largest compartment of mesenchyme in the intestine, that lead to fibrosis in Crohn's disease.
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What OpenQuestion holds
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.