ReviewExperimental & molecular medicine2026
From inflammation to fibrosis and cancer: the emerging role of AIEC-derived metabolites in intestinal disease progression.
Review in Experimental & molecular medicine, 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
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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
2 citing papers in PubMed.
- Failure of morphogenesis in chronic inflammation-associated early tumourigenesis: Extracellular matrix biomechanics as an integrative layer.Biochemistry and biophysics reports · 2026Review
- Microbial Signals in Cancer: Dissecting Host-Microbiota-Tumor Interactions and Potential Therapeutic Strategy.MedComm · 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
4 authors.
Funding
Abstract
The intestinal microbiota maintains mucosal homeostasis through dynamic host-microbe interactions. When this balance is disrupted, gut dysbiosis drives inappropriate immune activation, leading to dysregulated inflammation that contributes to the pathogenesis of chronic inflammatory diseases, including inflammatory bowel diseases (IBD). Chronic inflammation in patients with IBD increases the risk of intestinal fibrosis and colorectal cancer. However, therapeutic options for patients with IBD with fibrosis or neoplasia remain limited and challenging. Adherent-invasive Escherichia coli (AIEC) have emerged as key metabolic drivers of disease in IBD. We previously demonstrated that the AIEC-derived genotoxin colibactin and the siderophore yersiniabactin (Ybt) promote tumorigenesis through DNA damage and fibrosis via pro-fibrotic macrophage-fibroblast interactions, respectively. Because fibrosis and tumorigenesis involve overlapping pathways such as extracellular matrix remodeling, transforming growth factor-beta signaling, angiogenesis, and epithelial-to-mesenchymal transition, AIEC-derived metabolites may be functionally interconnected and could drive distinct pathological outcomes depending on the context of the disease. This Review highlights how AIEC-derived metabolites amplify inflammation, fibrosis, and neoplasia, outlines potential crosstalk between colibactin and Ybt, and discusses therapeutic opportunities targeting AIEC metabolite production in parallel with host-directed antifibrotic and cancer-prevention strategies.
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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.