ArticleJournal of inflammation research2025
Potential Functions and Causal Associations of GNLY in Primary Open-Angle Glaucoma: Integration of Blood-Derived Proteome, Transcriptome, and Experimental Verification.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Cross-Tissue Transcriptome-Wide Association Study and TWAS-FOCUS Fine-Mapping Reveal Novel Susceptibility Genes for Primary Open-Angle Glaucoma.Translational vision science & technology · 2026Article
- Large-Scaled Proteomics Analysis for Glaucoma: Integrated Genetics, Multi-Omics, UK Biobank and Therapeutic Analysis.Investigative ophthalmology & visual science · 2026Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Genome-wide association studies (GWAS) have identified multiple genetic loci associated with primary open-angle glaucoma (POAG). However, the mechanisms by which these loci contribute to POAG progression remain unclear. This study aimed to identify potential causative genes involved in the development of POAG. Methods: We utilized multi-dimensional high-throughput data, integrating proteome-wide association study(PWAS), transcriptome-wide association study (TWAS), and summary data-based Mendelian randomization (SMR) analysis. This approach enabled the identification of genes influencing POAG risk by affecting gene expression and protein concentrations in the bloodstream. The key gene was validated through enzyme-linked immunosorbent assay (ELISA) analysis. Results: PWAS identified 86 genes associated with altered blood protein levels in POAG patients. Of these, eight genes (SFTPD, CSK, COL18A1, TCN2, GZMK, RAB2A, TEK, and GNLY) were identified as likely causative for POAG ( Conclusion: This study reveals GNLY as a significant potential therapeutic target for managing primary open-angle glaucoma.
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.