Glaucoma Pathophysyology and Therapeutic Implication

Abstract

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 dysregulation, and toxic effects and oxidative damage cause by reactive oxygen species¹.

The aim of this article is to highlight the pathogenic role of vascular dysregulation and reactive oxygen species in POAG with the further possibilities for prevention and gene therapy.