Department of Experimental Medicine (DIMES), University of Genoa, 16126 Genoa, Italy.
IRCCS-Fondazione Bietti, 00198 Rome, Italy.
Int J Mol Sci. 2021 Jul 27;22(15):7994. doi: 10.3390/ijms22157994.
Retinal ganglion cells (RGCs) are a population of neurons of the central nervous system (CNS) extending with their soma to the inner retina and with their axons to the optic nerve. Glaucoma represents a group of neurodegenerative diseases where the slow progressive death of RGCs results in a permanent loss of vision. To date, although Intra Ocular Pressure (IOP) is considered the main therapeutic target, the precise mechanisms by which RGCs die in glaucoma have not yet been clarified. In fact, Primary Open Angle Glaucoma (POAG), which is the most common glaucoma form, also occurs without elevated IOP. This present review provides a summary of some pathological conditions, i.e., axonal transport blockade, glutamate excitotoxicity and changes in pro-inflammatory cytokines along the RGC projection, all involved in the glaucoma cascade. Moreover, neuro-protective therapeutic approaches, which aim to improve RGC degeneration, have also been taken into consideration.
视网膜神经节细胞（RGC）是中枢神经系统（CNS）的神经元群体，其胞体延伸至内视网膜，轴突延伸至视神经。青光眼是一组神经退行性疾病，其中 RGC 的缓慢进行性死亡导致视力永久性丧失。迄今为止，尽管眼内压（IOP）被认为是主要的治疗靶点，但导致青光眼 RGC 死亡的确切机制尚未阐明。事实上，原发性开角型青光眼（POAG）是最常见的青光眼形式，即使在眼压不高的情况下也会发生。本综述总结了一些病理情况，即轴突运输阻滞、谷氨酸兴奋性毒性以及沿 RGC 投射的促炎细胞因子的变化，这些都涉及青光眼级联反应。此外，还考虑了旨在改善 RGC 变性的神经保护治疗方法。
