ReviewFrontiers in immunology2025
Annexin A1 and A2 in inflammatory bowel disease pathogenesis: exploring new avenues for diagnosis and treatment.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Prognostic and Diagnostic Significance of Annexin A1 in ypT3 Locally Advanced Rectal Cancer Patients.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis, is a significant global health burden with gastrointestinal inflammation resulting from dysfunctional immune responses and chronic inflammation. This review synthesizes the roles of annexin A1 (AnxA1) and annexin A2 (AnxA2) in the pathophysiology of IBD, their diagnostic biomarkers, and therapeutic potential. AnxA1 interacts with FPR2/ALX receptors, inhibiting the release of pro-inflammatory cytokines and promoting epithelial cell repair. AnxA2 exhibits dual roles by interacting with S100A10. AnxA2 can induce NF-κB activation, promoting pro-inflammatory cytokine release and plasminogen activation. On the other hand, AnxA2 activates the TRAM-TRIF pathway, inhibiting NF-κB activation, promoting production of anti-inflammatory cytokines, fibrinolysis, and restoring tight junctions. Their modulation of NF-κB pathways shapes the molecular landscape of IBD. AnxA1 and AnxA2 are non-invasive plasma biomarkers that improve subtype-specific diagnostic accuracy compared to C-reactive protein. In the therapeutic context, AnxA1 mimetics and AnxA2 inhibitors reduce inflammation and promote healing, potentially in conjunction with anti-TNF drugs or nanoparticle delivery. Longitudinal studies and clinical trials are essential to identify the gaps in the standardization of testing and cytokine network interactions. AnxA1 and AnxA2 have the potential to transform the development of precise diagnostics and personalized therapies, redefining the management of IBD.
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.