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青光眼是一种以进行性视野缺损为特征的疾病,视网膜神经节细胞(RGCs)发生特征性退行性改变.热休克蛋白(HSP)属于应激蛋白超级家族,可在各种应急刺激下诱导产生.HSP具有分子伴侣、抗细胞凋亡和坏死功能,因此发挥着保护细胞的作用.近年来的基因多态性研究表明,HSP70表达的改变与原发性闭角及开角型青光眼均具有相关性,并对视神经、RGCs及小梁网细胞具有重要保护作用.病毒转染、替普瑞同和HSP90抑制剂17-AAG均可以人为诱导体内HSP70的表达,并抑制青光眼性视神经损伤.这些证据为治疗青光眼提供了新的思路.本文就近年来HSP70在青光眼发生和发展及治疗方面的研究进展进行综述.“,”Glaucoma is characterized by progressive loss of vision,which is caused by degeneration of retinal ganglion cells (RGCs).Heat shock proteins (HSP),whose expression could be induced by a variety of stressful stimuli,belong to a superfamily of stress proteins.Cell protective roles of HSPs are related to their chaperone functions,antiapoptotic and antinecrotic effects.In recent years,gene polymorphism studies have shown that changes in HSP70 expression are associated with primary angle-closure glaucoma and open angle glaucoma.Furthermore,emerging evidence reveals that HSP70 plays an important role in the protection of optic nerve,RGCs and trabecular meshwork cells.Animal experiment studies have shown that virus transfection,teprenone and HSP90 inhibitor 17-AAG could artificially induce the expression of HSP70 in vivo and prevent glaucomatous optic nerve from injury.These evidences provide new ideas of glaucoma treatment.This article aimed to review the current research progress of HSP70 in the pathogenesis,progression and treatment of glaucoma.