Language

English

Publication Date

1-9-2024

Journal

Nature Communications

DOI

10.1038/s41467-023-44380-y

PMID

38195602

PMCID

PMC10776627

PubMedCentral® Posted Date

1-9-2024

PubMedCentral® Full Text Version

Post-print

Abstract

Primary open-angle glaucoma (POAG), characterized by retinal ganglion cell death, is a leading cause of irreversible blindness worldwide. However, its molecular and cellular causes are not well understood. Elevated intraocular pressure (IOP) is a major risk factor, but many patients have normal IOP. Colocalization and Mendelian randomization analysis of >240 POAG and IOP genome-wide association study (GWAS) loci and overlapping expression and splicing quantitative trait loci (e/sQTLs) in 49 GTEx tissues and retina prioritizes causal genes for 60% of loci. These genes are enriched in pathways implicated in extracellular matrix organization, cell adhesion, and vascular development. Analysis of single-nucleus RNA-seq of glaucoma-relevant eye tissues reveals that the POAG and IOP colocalizing genes and genome-wide associations are enriched in specific cell types in the aqueous outflow pathways, retina, optic nerve head, peripapillary sclera, and choroid. This study nominates IOP-dependent and independent regulatory mechanisms, genes, and cell types that may contribute to POAG pathogenesis.

Keywords

Humans, Genome-Wide Association Study, Glaucoma, Open-Angle, Gene Expression Regulation, Causality, Glaucoma, Functional genomics, Statistical methods, Optic nerve diseases

Published Open-Access

yes

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