ReviewAnnals of medicine2025
Beyond inflammation: what drives the self-perpetuating cycle of fibrosis in IBD?
Review in Annals of medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- A self-crosslinkable, adhesive intestine-derived extracellular matrix hydrogel enhances organoid retention and restores intestinal barrier integrity.Bioactive materials · 2027Article
- Response to letter regarding "beyond inflammation: what drives the self-perpetuating cycle of fibrosis in IBD?"Annals of medicine · 2026Article
- The Aging Microenvironment Shapes Angiogenic Remodeling in IBD-Associated Colorectal Carcinogenesis.Aging cell · 2026Review
- Regarding: 'beyond inflammation: what drives the self-perpetuating cycle of fibrosis in IBD?'Annals of medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intestinal fibrosis is a major complication of inflammatory bowel disease (IBD). While inflammation is a prerequisite for initiating fibrosis, it does not fully explain its progression, which often continues despite effective anti-inflammatory treatment. This suggests that fibrotic mechanisms evolve from an inflammation-dependent priming phase to a self-perpetuating phase that can operate independently of ongoing inflammation. While the former has been widely studied, the latter remains underexplored. In this context, this review summarizes the current evidence on the self-perpetuating mechanisms driving fibrosis in IBD, even after inflammation resolves. We delve into key drivers such as genetic predisposition, extracellular matrix microenvironment, creeping fat, and metabolic reprogramming. The aim is to enhance understanding of this self-sustaining cycle and encourage further research to advance treatment strategies for IBD-related fibrosis.
Indexed as
Identifiers
What Socratic 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 Socratic graph.