ReviewJournal of gastroenterology2025
Main genetic factors associated with inflammatory bowel diseases and their consequences on intestinal permeability: involvement in gut inflammation.
Review in Journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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
18 citing papers in PubMed.
- From Multi-Omics to Molecular Causality: A Five-Tier Evidence Framework for the Single-Bacterium-Metabolite Axis in IBD.Microorganisms · 2026Review
- Emergency granulopoiesis and innate immune memory in inflammatory bowel disease.Trends in immunology · 2026Review
- Review
- Therapeutic zinc targets dysregulated GC-C signaling and restores ileal defects in a preclinical model of familial diarrheal disease.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Review
- Current approaches to disease severity and therapy effectiveness assessment in patients with inflammatory bowel disease.World journal of gastrointestinal pharmacology and therapeutics · 2026Review
- Vitamin D Receptor-Macrophage-IL-23 Axis in Inflammatory Bowel Disease: Pathogenic Mechanisms and Therapeutic Hope.Journal of clinical medicine · 2026Review
- Hydrodynamic Delivery of IL-10 Gene for Local Immunomodulation in Human Crohn's Disease Tissue: A Proof-of-Concept Study.Pharmaceutics · 2026Article
- Flos sophorae immaturus exosome-like nanovesicles alleviate ulcerative colitis by attenuating intestinal oxidative stress and inflammation through activating Aryl hydrocarbon receptor via gut microbiota and tryptophan metabolism regulation.Journal of nanobiotechnology · 2026Article
- Mitophagy in inflammatory bowel disease: regulatory mechanisms and therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Integrative single-cell transcriptomics and mendelian randomization identifies BTN3A2 as a shared protective factor in Behçet's disease and inflammatory bowel disease.Frontiers in immunology · 2026Article
- Agricultural chemicals and gut microbiota dysbiosis: implications for the pathogenesis of inflammatory bowel disease.Frontiers in nutrition · 2026Review
- Identification of TIMP1 as a Key Regulator of Ferroptosis in Ulcerative Colitis Through Bioinformatics and Functional Experiments.Gastroenterology research and practice · 2026Article
- Endoplasmic reticulum stress as a mechanistic link between nutrition and inflammatory bowel disease.Frontiers in nutrition · 2026Review
- Crohn's disease: research progress in decoding pathogenic multi-network and precision management of artificial intelligence radiomics.Frontiers in immunology · 2026Review
- Article
- Gut microbiota and inflammatory bowel disease: mechanisms, clinical implications, and future directions.Molecular biology reports · 2025Review
- Roles of Deubiquitinases OTUD3 and OTUD5 in Inflammatory Bowel Diseases.International journal of molecular sciences · 2025Review
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
Crohn's disease (CD) and ulcerative colitis (UC), the two main subtypes of inflammatory bowel diseases (IBD), are chronic relapsing inflammatory disorders of the gastrointestinal tract. IBD are multifactorial diseases with a complex etiology, involving an intricate interaction between environmental and genetic factors. Since the discovery of NOD2 gene in 2001, genome-wide association studies have reported more than 200 IBD susceptibility loci. The strongest associations highlighted five main pathways as altered in IBD: bacterial sensing (NOD2), autophagy (ATG16L1, IRGM…), endoplasmic reticulum stress (XBP1, ARG2…), Th-17 immune pathway (IL23-receptor), and the vitamin D receptors (VDR). The pathophysiology of IBD results from an abnormal immune response toward an altered gut microbiota. Although the primum movens remains unknown, an increased intestinal permeability is clearly involved in the genesis of this abnormal crosstalk, leading to whole tissue inflammation. Thus, an excessive intestinal permeability, or "leaky gut", has been described to precede the development of CD. Moreover, in IBD, intestinal permeability is described to be a sensitive prognostic indicator of relapse in patients with quiescent IBD. Thus, the aim of this review is to highlight the molecular and cellular mechanisms by which the main pathways associated with IBD could contribute to alter the intestinal permeability to favour and/or exacerbate chronic inflammation, leading to debilitating diseases.
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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.