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. Author manuscript; available in PMC: 2024 Jul 1.
Published in final edited form as: Ophthalmology. 2023 Feb 20;130(7):756–763. doi: 10.1016/j.ophtha.2023.02.018

Figure 1. Roles of the TXNRD2 and ME3 genes in the mitochondria and a possible functional mechanism for disease-associated single nucleotide polymorphisms (SNPs) in primary open-angle glaucoma (POAG) pathogenesis.

Figure 1.

(A) The ME3 gene encodes a protein that catalyzes the production of NADPH from NADP+, while the TXNRD2 gene encodes a protein that consumes NADPH in the mitochondria. (B) POAG-associated SNPs in TXNRD2 and ME3 may lead to lower levels of NADPH, a key mitochondrial antioxidant. This would result in increased reactive oxygen species and oxidative stress. Oxidative stress has been shown to cause dysfunctional aqueous outflow through the trabecular meshwork (TM) and elevated intraocular pressure (IOP). Additionally, mitochondrial dysfunction and oxidative stress can cause toxic injury to retinal ganglion cells (RGCs) independent of IOP.