Ster Anda Maria, Popp Radu Anghel, Petrisor Felicia Maria, Stan Cristina, Pop Victor Ioan
Dept. of Ophthalmology, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Dept. of Medical Genetics, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Clujul Med. 2014;87(3):143-6. doi: 10.15386/cjmed-295. Epub 2014 Aug 5.
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.
原发性开角型青光眼(POAG)是一种慢性、不可逆的视神经病变,可导致视网膜神经节细胞逐渐死亡,临床上表现为无症状的视野缺损以及颜色和对比敏感度下降。已经提出了多种致病理论,其中一些已被证实与疾病发展有关:眼压升高导致的机械损伤、视神经的易感性差异、特定核基因的突变、谷氨酸水平升高、一氧化氮(NO)代谢改变、线粒体基因组变化、血管紊乱以及活性氧引起的毒性作用和氧化损伤[1]。本文的目的是强调血管紊乱和活性氧在POAG中的致病作用以及预防和基因治疗的进一步可能性。