ArticleTranslational vision science & technology2025
Druggable Genome Mendelian Randomization and GWAS-sceQTLs MR Analysis Reveal Genetic Associations Between Open-Angle Glaucoma and Immune Cells, and Identify Potential Drugs.
Article in Translational vision science & technology, 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.
- Druggable genome-wide Mendelian randomization analysis identifies potential treatment targets in vascular dementia.Alzheimer's & dementia (New York, N. Y.)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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The purpose of this study was to identify therapeutic targets and repurposable drugs for primary open-angle glaucoma (POAG) by investigating its immunometabolic mechanisms using druggable genomic and single-cell transcriptomic approaches. Methods: We integrated druggable genome-wide and single-cell Mendelian randomization (MR) using POAG genome-wide association study (GWAS) data, blood and single-cell expression quantitative trait loci (eQTL) datasets. Causal genes were identified via colocalization and MR inference (inverse-variance weighted [IVW]). Drug-gene interactions were predicted using molecular docking (DSigDB/CB-Dock2), and safety was assessed via phenome-wide association studies (PheWAS). Results: (1) Identified two POAG causal genes: risk genes YWHAG (odds ratio [OR] = 1.207, 95% confidence interval [CI] = 1.131-1.288) and protective genes GFPT1 (OR = 0.874, 95% CI = 0.840-0.910). (2) Cell-type-specific paradoxical effect: In CD4+KLRB1-T cells, high GFPT1 expression increased POAG risk (OR = 1.448, 95% CI = 1.241-1.690, P = 2.545 × 10-6), suggesting its role in driving immunometabolic reprogramming via the hexosamine biosynthesis pathway (HBP). (3) Drug screening: Molecular docking confirmed strong binding of trimipramine, desipramine, and cyclosporin to GFPT1 (Vina score < -5), with PheWAS indicating no significant off-target effects. Conclusions: GFPT1 in CD4+ memory T cells contributes to POAG pathogenesis through immunometabolic dysregulation. Three existing drugs identify potential for therapeutic repurposing. Translational Relevance: This study identifies GFPT1-driven immunometabolic dysfunction as a novel target in POAG and nominates three US Food and Drug Administration (FDA)-approved drugs for immediate clinical translation, accelerating the path to trials.
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.