ReviewChinese medical journal2025
Intestinal fibrosis associated with inflammatory bowel disease: Known and unknown.
Review in Chinese medical journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed.
- Phenotypic switching of gastrointestinal smooth muscle cells and the regulatory role of macrophages: a literature review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- IL11+ fibroblasts are implicated in nonresponse to anti-TNF-α via fibrosis in inflammatory bowel disease.JCI insight · 2026Article
- The Aging Microenvironment Shapes Angiogenic Remodeling in IBD-Associated Colorectal Carcinogenesis.Aging cell · 2026Review
- Layer-by-layer engineered outer membrane vesicles enable oral upadacitinib delivery for inflammation control and fibrosis attenuation in ulcerative colitis.Journal of nanobiotechnology · 2026Article
- TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- MicroRNA‑microbiome cross‑kingdom networks drive inflammatory bowel disease through dynamic regulatory ecosystems (Review).International journal of molecular medicine · 2026Review
- Fecal microbiota transplantation alleviates DSS-induced colitis: increased fecal butyrate, reduced colonic p65 phosphorylation, and altered Th17/Treg ratios in the spleen and mesenteric lymph nodes.Frontiers in immunology · 2026Article
- The Paradox of NET Involvement in the Pathogenesis of Inflammatory Bowel Disease.Inflammatory bowel diseases · 2026Review
- Generative AI-augmented transcriptomic and microbiome analysis across inflammatory and fibrotic disease states in Crohn's disease.Frontiers in artificial intelligence · 2026Article
- Immune-Mediated Gut-Lung Axis in IPF: Bidirectional Mendelian Randomization and Mediation Analysis of Microbiota, Inflammatory Proteins, and Metabolites.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Article
- Endoplasmic reticulum stress and exosomes secretion in the pathogenesis of inflammatory bowel disease: a concise summary of research findings.Frontiers in pharmacology · 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractIntestinal fibrosis is a major complication of inflammatory bowel disease (IBD), leading to a high incidence of surgical interventions and significant disability. Despite its clinical relevance, no targeted pharmacological therapies are currently available. This review aims to explore the underlying mechanisms driving intestinal fibrosis and address unresolved scientific questions, offering insights into potential future therapeutic strategies. We conducted a literature review using data from PubMed up to October 2024, focusing on studies related to IBD and fibrosis. Intestinal fibrosis results from a complex network involving stromal cells, immune cells, epithelial cells, and the gut microbiota. Chronic inflammation, driven by factors such as dysbiosis, epithelial injury, and immune activation, leads to the production of cytokines like interleukin (IL)-1β, IL-17, and transforming growth factor (TGF)-β. These mediators activate various stromal cell populations, including fibroblasts, pericytes, and smooth muscle cells. The activated stromal cells secrete excessive extracellular matrix components, thereby promoting fibrosis. Additionally, stromal cells influence the immune microenvironment through cytokine production. Future research would focus on elucidating the temporal and spatial relationships between immune cell-driven inflammation and stromal cell-mediated fibrosis. Additionally, investigations are needed to clarify the differentiation origins of excessive extracellular matrix-producing cells, particularly fibroblast activation protein (FAP) + fibroblasts, in the context of intestinal fibrosis. In conclusion, aberrant stromal cell activation, triggered by upstream immune signals, is a key mechanism underlying intestinal fibrosis. Further investigations into immune-stromal cell interactions and stromal cell activation are essential for the development of therapeutic strategies to prevent, alleviate, and potentially reverse 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.