| Summary: | Oxidative stress and neuroinflammation are involved in the pathogenesis and progression of glaucoma. Our aim was to evaluate the impact of selected single-nucleotide polymorphisms in inflammation and oxidative stress genes on the risk of glaucoma, the patients’ clinical characteristics and the glaucoma phenotype. In total, 307 patients with primary open-angle glaucoma or ocular hypertension were enrolled. The control group included 339 healthy Slovenian blood donors. DNA was isolated from peripheral blood. Genotyping was performed for <i>SOD2</i> rs4880, <i>CAT</i> rs1001179, <i>GPX1</i> rs1050450, <i>GSTP1</i> rs1695, <i>GSTM1</i> gene deletion, <i>GSTT</i>1 gene deletion, <i>IL1B</i> rs1143623, <i>IL1B</i> rs16944, <i>IL6</i> rs1800795 and <i>TNF</i> rs1800629. We found a nominally significant association of <i>GSTM1</i> gene deletion with decreased risk of ocular hypertension and a protective role of <i>IL1B</i> rs16944 and <i>IL6</i> rs1800629 in the risk of glaucoma. The CT and TT genotypes of <i>GPX1</i> rs1050450 were significantly associated with advanced disease, lower intraocular pressure and a larger vertical cup–disc ratio. In conclusion, genetic variability in <i>IL1B</i> and <i>IL6</i> may be associated with glaucoma risk, while <i>GPX</i> and <i>TNF</i> may be associated with the glaucoma phenotype. In the future, improved knowledge of these pathways has the potential for new strategies and personalised treatment of glaucoma.
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