青光眼动物模型中自噬与视网膜神经节细胞的关系

摘要

青光眼的主要病理特征是视网膜神经节细胞(RGCs)渐进性丢失,而其损伤机制尚未明确.自噬是溶酶体降解物质的过程,该过程消除了受损的细胞成分,包括细胞器和长寿蛋白,这对维持细胞内环境的稳定有着重要作用.最近的研究表明,自噬参与了青光眼发病的病理生理过程.本文总结了视神经损害模型、视网膜缺血-再灌注模型、高眼压模型等不同青光眼动物模型中自噬与RGCs的关系,发现在不同青光眼动物模型中,自噬既可促进RGCs存活,又可促进其死亡,而在相同动物模型中,自噬对RGCs的调节也发挥着双刃剑的作用.同时阐述了自噬与具有神经元保护作用的Sirt1之间的相互作用.%The main pathological feature of glaucoma is progressive loss of retinal ganglion cells (RGCs),and the damage mechanisms have not been elucidated.Autophagy is a lysosomal degradative process that eliminates damaged cellular constituents,including organelles and long-life proteins.And autophagy plays an important role in cellular homeostasis.Recent studies have shown that autophagy is involved in the pathophysiological process of glaucoma.This article summarized the relationship between autophagy and RGCs in different animal models of glaucoma,such as optic nerve damage model,ischemia-reperfusion model and ocular hypertension model.In various animal models of glaucoma,autophagy can not only promote RGCs survival but also their death.And in the same animal model of glaucoma,autophagy also plays a double-edged sword effect on RGCs.Meanwhile,we elaborated the interaction between autophagy and Sirt1,which can protect the neurons.