ReviewInternational urogynecology journal2026
Molecular Signatures of Bladder Pain Syndrome: A Systematic Review Towards Phenotype-Informed Diagnostics.
Review in International urogynecology journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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Who cites it
0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introduction and hypothesisBladder painsyndrome (BPS) is a disabling condition diagnosed clinically, characterised by marked heterogeneity in cystoscopic phenotype and treatment response. Molecular mechanisms remain incompletely defined, and no validated biomarkers currently support diagnosis or phenotypic stratification. The objective was to synthesise molecular evidence underpinning BPS and evaluate biomarker candidates relevant to phenotype-informed diagnostics.
methodsA Preferred Reporting Items for Systematic reviews and Meta-Analyses-guided search of PubMed and the Cochrane Library (to 24 November 2024) identified human and experimental studies reporting molecular, transcriptomic, proteomic or biochemical characterisation of BPS (including studies indexed under interstitial cystitis). Eligibility followed the SPIDER framework. Owing to heterogeneity in phenotyping, biospecimens and analytical platforms, findings were narratively synthesised and organised by mechanistic domain.
resultsTwenty studies were included (316 records screened). Convergent findings supported four inter-related domains: immune activation and lymphoid recruitment, including IL6, TNF, CXCL13/CXCR5 and IL17RA-linked signalling; urothelial barrier impairment with reduced CDH1 and TJP1 and increased adhesion molecules (e.g. ICAM1); neurogenic sensitisation involving NGF, ADCYAP1 and CNR1; and inflammasome and oxidative pathways, including NLRP3, IL1B and NOS2. Where phenotypes were distinguished, Hunner-type BPS demonstrated an immune- and endoplasmic-reticulum-stress-enriched profile compared with non-Hunner disease. Across studies, biomarker signals showed limited reproducibility, constrained by small cohorts and inconsistent phenotyping.
conclusionsCurrent evidence supports BPS as a syndrome comprising biologically distinct endotypes spanning immune, epithelial, neurogenic and inflammasome pathways. Large, rigorously phenotyped human studies using harmonised multi-omics approaches are required to validate biomarkers and enable phenotype-informed diagnosis and targeted therapy.
Indexed as
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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.