ReviewFrontiers in immunology2026
Signaling pathways related to interstitial cystitis.
Review in Frontiers in immunology, 2026. 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.
- Fucoidan from Fucus Vesiculosus Alleviates Interstitial Cystitis by Suppressing the AKT/NLRP3 Inflammasome Axis.Pharmaceuticals (Basel, Switzerland) · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interstitial cystitis/bladder pain syndrome (IC/BPS) represents a chronic, non-infectious inflammatory bladder disorder, predominantly affecting women. Primary symptoms include ongoing pelvic pain, frequent urination, and urgency, often accompanied by functional somatic pain syndromes and psychological health disturbances. The severity of IC symptoms significantly impairs patients' quality of life, highlighting the necessity for research on the pathogenesis, progression, and treatment of IC/BPS. Although the exact etiology of IC remains unclear, and there is no simple or definitive diagnostic method, current clinical treatments primarily focus on symptom relief rather than a cure. In recent years, extensive experimental studies on the etiology and pathophysiology of IC have identified a multitude of signaling pathways involved in the disease's initiation, progression, and self-repair mechanisms. This study focuses on IC-related signaling pathways, analyzing the role of key molecular signals in the onset and progression of IC. By integrating clinical symptoms and signs with molecular biology insights, we provide a comprehensive overview and comparative analysis of IC's etiology and pathophysiological activities. The goal is to establish a theoretical foundation for the development of more efficient diagnostic tools, drug therapies, treatment evaluations, and preventive strategies for IC.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.