GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE301nnn/GSE301522/primaryOK200OtherHomo sapiensOtherhttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE301522GEOGSEfalseChromatin topology dynamics of dexamethasone-treated trabecular meshwork identifies 78 causal genes for intraocular pressure and primary open angle glaucoma [HiC]The physiology of trabecular meshwork (TM) controls aqueous humor outflow resistance and thereby intraocular pressure (IOP), a major risk factor for primary open-angle glaucoma (POAG). To decipher how GWAS-identified non-coding variants contribute to IOP and POAG, we generated a high-resolution map of genome topology and regulatory modules from primary human TM cell lines. Integrated analyses with dexamethasone-treated TM cells, a model of augmented IOP, demonstrate extensive changes in chromatin compartments, accessibility, looping, and histone marks that are highly concordant with transcriptional changes. By combining GWAS-associated variants with dexamethasone-induced chromatin looping, we discovered 26 IOP- and 52 POAG- candidate causal genes, belonging to key TM pathways, including integrin, transcriptional regulation of VENTX, and TNF signaling. Our studies provide a mechanistic framework for elucidating genetic complexity of IOP and pathogenesis of POAG and suggest new targets for therapies.2026/04/10GSE301522GSM9084754GSM9084732GSM9084733GSM9084755GSM9084730GSM9084752GSM9084753GSM9084731GSM9084736GSM9084758GSM9084759GSM9084737GSM9084756GSM9084734GSM9084757GSM9084735GSM9084738GSM9084739GSM9084761GSM9084740GSM9084760GSM9084743GSM9084744GSM9084741GSM9084742GSM9084747GSM9084725GSM9084748GSM9084726GSM9084745GSM9084724GSM9084746GSM9084729GSM9084727GSM9084749GSM9084728GSM9084750GSM908475130173301522Homo sapiens[41890121]