糖尿病视网膜病变过程中神经节细胞内质网应激的研究进展

Advances in research of endoplasmic reticulum stress of ganglion cells in diabetic retinopathy

糖尿病性视网膜病变(DR)是糖尿病患者视力下降和致盲的重要原因。早在糖尿病视网膜微血管损伤出现之前就已发生了神经退行性变,主要表现为神经节细胞凋亡等,而内质网应激(ERS)参与了这一过程。当细胞稳态异常,未折叠或错误折叠的蛋白质在内质网内累积,细胞就会启动自我拯救程序,即未折叠蛋白反应(UPR)O UPR具有三条信号通路:ATF6信号通路、PERK信号通路以及IRE1信号通路。UPR与DR进程中的氧化应激、炎症、细胞凋亡、血-视网膜屏障破坏和血管生成密切相关。深入探索ERS与DR神经节细胞损伤的内在机制,对于寻找新的有效药物预防或治疗糖尿病视网膜病变十分有意义。

Diabetic retinopathy (DR) is an important cause of vision loss and blindness in diabetic patients. Studies have shown that neurodegenerative changes have occurred before diabetic retinal microvascular injury,such as reactive glial increase and ganglion cell apoptosis,and endoplasmic reticulum stress is involved in this process.Studies have shown that neurodegenerative changes have occurred before diabetic retinal microvascular injury,mainly as ganglion cell apoptosis,and endoplasmic reticulum stress is involved in this process.The UPR has three signal paths:the ATF6 signal path,the PERK signal path,and the IRE1 signal path.It is closely related to oxidative stress,inflammation,apoptosis,BRB destruction and angiogenesis in the DR process.Exploring the intrinsic mechanism of ERS and ganglion cell injury is of great significance for finding new effective drugs to prevent or treat diabetic patients.