ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
Inflammatory bowel disease and extracellular matrix: when victim becomes double agent.
Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- Cellular crosstalk of fibroblast-myofibroblast transition in intestinal homeostasis and disease.Biomarker research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe extracellular matrix (ECM) represents an intricate network of proteins present in all organs, with specific physical and biochemical functions. ECM is composed of two distinct but connected entities: the basement membrane, located beneath the epithelium, and the interstitial matrix, present in the mucosa and submucosa. Physiologically, ECM modulates several functions, including epithelium turnover, intercellular communications, cell adhesion, differentiation, proliferation, apoptosis, and tissue remodeling.
findingsAfter an injury, the epithelial barrier fails, affecting the ECM structure and functions. The normal gut structure and functions depend on ECM, which is regulated by ECM-producing cells/ECM-degrading enzymes. Intestinal injury can lead to epithelial barrier disruption and then to acute mucosal inflammation that can heal or become chronic. The ECM is directly involved in mucosal healing, while the key mechanisms leading to the chronicity of intestinal inflammation are unknown. Inflammatory cells release countless cytokines, chemokines, and growth factors, which, by interacting with specific components of the ECM, induce an overactivation of the immune system. In this context, ECM represents an important player in inflammatory diseases, including the inflammatory bowel diseases (IBD) and related complications such as intestinal fibrosis. In the last years, progressive advancements in the knowledge of IBD pathogenesis have provided crucial information for the discovery of new treatments. Nevertheless, few studies investigate the ECM's multiple roles in the sustenance and the exacerbation of the immune reaction.
conclusionThis review aims to emphasize the dynamic aspects of the ECM, giving an overview of its direct involvement in intestinal inflammatory diseases and the related intestinal fibrosis.
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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.