ArticleWorld journal of gastroenterology2012
Cellular and molecular mechanisms of intestinal fibrosis.
Article in World journal of gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 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.
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
142 citing papers in PubMed, 1 synthesis or guideline pooled it, 267 citations in OpenAlex.
- Pooled it
- Results of Multicenter Phase II Study With Imatinib Mesylate in Allogeneic Recipients With Steroid-Refractory Chronic GVHD.Cell transplantationTrial
- Nitric Oxide in the Intestinal Stem Cell Niche: A Spatial Model of Nitrosative Stress and Clonal Evolution in Colitis-Associated Colorectal Cancer.Digestive diseases and sciences · 2026Review
- Differential Protective Actions of Dulaglutide and Dexamethasone in Methotrexate Induced Pulmonary Fibrosis: Relationship with AMPK and Beclin-1 Levels.Biomedicines · 2026Article
- Phenotypic Heterogeneity in Crohn's Disease-Associated Intestinal Strictures: An Exploratory Retrospective Cohort Study.Diagnostics (Basel, Switzerland) · 2026Article
- Ulcerative colitis, pathophysiological mechanisms and drug repurposing: a new therapeutic dawn-narrative review.Inflammopharmacology · 2026Review
- Developing a protocol to counteract spontaneous in vitro activation of intestinal fibroblasts using design of experiments.npj biomedical innovations · 2026Article
- Microbial collagenase activity is linked to oral-gut translocation in advanced chronic liver disease.Nature microbiology · 2026Article
- Macrophage Immune-Competent Colon Assembloids for Functional Interrogation of Neuroinflammation-Induced Colonic Dysmotility.Gastro hep advances · 2026Article
- Intestinal Stenosis Related to Immune Checkpoint Inhibitors Caused by Sintilimab: A Case Report.Journal of inflammation research · 2026Article
- An intricate relationship between fibrosis and autoimmune diseases: a specific focus on unraveling its molecular, immunological, and epigenetic drivers.Frontiers in immunology · 2026Review
- Intestinal subepithelial myofibroblasts in inflammatory bowel disease: fibroblast heterogeneity, fibrosis, and therapeutic targeting.Frontiers in medicine · 2026Review
- Activation of the RSAD2-YTHDF1 axis in smooth muscle causes inflammatory bowel disease via intercellular mitochondrial transfer.Nature communications · 2025Article
- Beyond inflammation: what drives the self-perpetuating cycle of fibrosis in IBD?Annals of medicine · 2025Review
- Review
- Article
- Insights into the Molecular Mechanisms and Novel Therapeutic Strategies of Stenosis Fibrosis in Crohn's Disease.Biomedicines · 2025Review
- 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
82 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Fibrosis is a chronic and progressive process characterized by an excessive accumulation of extracellular matrix (ECM) leading to stiffening and/or scarring of the involved tissue. Intestinal fibrosis may develop in several different enteropathies, including inflammatory bowel disease. It develops through complex cell, extracellular matrix, cytokine and growth factor interactions. Distinct cell types are involved in intestinal fibrosis, such as resident mesenchymal cells (fibroblasts, myofibroblasts and smooth muscle cells) but also ECM-producing cells derived from epithelial and endothelial cells (through a process termed epithelial- and endothelial-mesenchymal transition), stellate cells, pericytes, local or bone marrow-derived stem cells. The most important soluble factors that regulate the activation of these cells include cytokines, chemokines, growth factors, components of the renin-angiotensin system, angiogenic factors, peroxisome proliferator-activated receptors, mammalian target of rapamycin, and products of oxidative stress. It soon becomes clear that although inflammation is responsible for triggering the onset of the fibrotic process, it only plays a minor role in the progression of this condition, as fibrosis may advance in a self-perpetuating fashion. Definition of the cellular and molecular mechanisms involved in intestinal fibrosis may provide the key to developing new therapeutic approaches.
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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.