ArticleInflammatory bowel diseases2013
Increased activation of latent TGF-β1 by αVβ3 in human Crohn's disease and fibrosis in TNBS colitis can be prevented by cilengitide.
Article in Inflammatory bowel diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 62 citations in OpenAlex.
- The inflammatory/fibrotic axis across organs: myelofibrosis as a model of reversibility.JCI insight · 2026Review
- Intestinal subepithelial myofibroblasts in inflammatory bowel disease: fibroblast heterogeneity, fibrosis, and therapeutic targeting.Frontiers in medicine · 2026Review
- Macrophage-Orchestrated Metabolic Sensing Drives IBD Pathogenesis: A Framework for Targeted Therapy.International journal of biological sciences · 2026Review
- Muscular hyperplasia in Crohn's disease strictures: through thick and thin.American journal of physiology. Cell physiology · 2024Review
- Overcoming Vemurafenib Resistance in Metastatic Melanoma: Targeting Integrins to Improve Treatment Efficacy.International journal of molecular sciences · 2024Article
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Current Approach to Risk Factors and Biomarkers of Intestinal Fibrosis in Inflammatory Bowel Disease.Medicina (Kaunas, Lithuania) · 2024Review
- Cellular and Molecular Mechanisms of Intestinal Fibrosis.Gut and liver · 2023Review
- Serum TGF-Journal of immunology research · 2023Article
- The causal associations between growth factors and constipation: a two-sample Mendelian randomization study.Frontiers in physiology · 2023Article
- Structure-Based Discovery of a Novel Class of Small-Molecule Pure Antagonists of Integrin αVβ3.Journal of chemical information and modeling · 2022Article
- Therapeutic Potential of the Combination of Pentoxifylline and Vitamin-E in Inflammatory Bowel Disease: Inhibition of Intestinal Fibrosis.Journal of clinical medicine · 2022Article
- Review
- Mesenchymal Stem/Stromal Cells in Progressive Fibrogenic Involvement and Anti-Fibrosis Therapeutic Properties.Frontiers in cell and developmental biology · 2022Review
- The Multiple Faces of Integrin-ECM Interactions in Inflammatory Bowel Disease.International journal of molecular sciences · 2021Review
- Connective Tissue Disorders and Cardiovascular Complications: The Indomitable Role of Transforming Growth Factor-β Signaling.Advances in experimental medicine and biology · 2021Article
- A KDM4-DBC1-SIRT1 Axis Contributes to TGF-b Induced Mesenchymal Transition of Intestinal Epithelial Cells.Frontiers in cell and developmental biology · 2021Article
- Cilengitide Inhibits Neovascularization in a Rabbit Abdominal Aortic Plaque Model by Impairing the VEGF Signaling.BioMed research international · 2021Article
- Article
- Mechanism of fibrosis and stricture formation in Crohn's disease.Scandinavian journal of immunology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundStrictures develop in >30% of patients affected with Crohn's disease. No available medication prevents stricture development in susceptible patients. In Crohn's strictures, but not adjacent normal intestine, TGF-β1 increases in muscularis smooth muscle, increasing collagen I production and strictures. Muscle cells express αVβ3 integrin containing an Arg-Gly-Asp (RGD) binding domain. The aim was to determine whether increased TGF-β1 levels in strictures were the result of latent TGF-β1, which contains an RGD sequence, binding to and activation by αVβ3; and whether cilengitide, which is an RGD-containing αVβ3 integrin inhibitor, decreases TGF-β1 activation and development of fibrosis in chronic 2,4,6 trinitrobenzene sulfonic acid (TNBS)-induced colitis.
designMuscle cells isolated from Crohn's disease strictures and normal resection margin and from the colon of rats after 42 days of chronic TNBS-induced colitis were used to prepare RNA and protein lysates and to initiate primary cultures. The mechanisms leading to increased TGF-β1 activation, collagen I production, and fibrosis were examined in human muscle and in rats. Human cultured cells in vitro and rats in vivo were treated with cilengitide to determines it efficacy to decrease TGF-β1-activation, collagen production, and decrease the development of fibrosis.
resultsLatent TGF-β1 is activated by the αVβ3 RGD domain in human and rat intestinal smooth muscles. Increased activation of TGF-β1 in Crohn's disease and in TNBS-induced colitis causes increased collagen production, and fibrosis that could be inhibited by cilengitide.
conclusionsCilengitide, an αVβ3 integrin RGD inhibitor, could be a novel treatment to diminish excess TGF-β1 activation, collagen I production, and development of fibrosis in Crohn's disease.
Indexed as
Identifiers
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.