Primary Open Angle Glaucoma (POAG) is a chronic, irreversible optic neuropathy leading to the progressive death of retinal ganglion cells, clinically observed as silent visual field loss along with a decrease in colour and contrast sensitivity. Multiple pathogenic theories have been issued and some of them have proven their involvement in disease development: mechanical damage due to increased intraocular pressure, variable susceptibility of the optic nerve, mutation in specific nuclear genes, increased glutamate levels, alteration in nitric oxide (NO) metabolism, changes in the mitochondrial genome, vascular disturbances, and toxic effects and oxidative damage caused by reactive oxygen species [1]. The aim of this article is to highlight the pathogenic role of vascular disturbances and reactive oxygen species in POAG with the further possibilities for prevention and gene therapy.
Keywords: genetic risk factors; glutathion; nitric oxide; oxidative stress; primary open angle glaucoma.