| Summary: | Rho-associated coiled-coil kinase (ROCK) signaling can affect glaucoma risk by regulating trabecular meshwork outflow. We investigated the effect of <i>ROCK</i> gene polymorphism on the risks of primary open-angle glaucoma (POAG) and POAG-related phenotypes including intraocular pressure (IOP) in a Korean population. A total of 24 single-nucleotide polymorphisms (SNPs) from <i>ROCK1</i> and <i>ROCK2</i> were selected and genotyped for 363 POAG patients and 213 healthy controls. Among the 363 POAG patients, 282 were normal-tension glaucoma (NTG, baseline IOP ≤ 21 mmHg) and 81 were high-tension glaucoma (HTG, baseline IOP > 21 mmHg). The SNPs rs288979, rs1006881, rs35996865, rs10083915, and rs11873284 in <i>ROCK1</i> (tagged to each other, <i>r</i><sup>2</sup> = 1) were nominally associated with risk of HTG (OR = 0.52, <i>p</i> = 0.045). However, there were no SNPs that were significantly associated with the risk of NTG. In the genotype-phenotype correlation analysis, the SNPs rs2230773 and rs3771106 in <i>ROCK2</i> were significantly correlated with central corneal thickness (CCT)-adjusted IOP (<i>p</i> = 0.024) and axial length (AXL; <i>p</i> = 0.024), respectively. The present data implicated the role of <i>ROCK</i> in POAG development, and as such, can serve as a good reference for upcoming Rho/ROCK-pathway-related studies on POAG.
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