谷氨酸与视网膜神经节细胞凋亡的研究进展

Research Progress in Glutamic Acid and Retinal Ganglion Cell Apoptosis

视网膜神经节细胞(RGCs)进行性的死亡和丢失是青光眼导致视功能损害的基础病理。RGCs的死亡是通过细胞凋亡的形式进行的。RGCs损伤后,多种原因导致的细胞外谷氨酸在正常水平之上大量聚集,通过谷氨酸受体引起细胞内Ca2+增加,继而进入一系列细胞凋亡途径。局部的谷氨酸聚集还会引起半胱天冬酶及肿瘤坏死因子α的增加,共同参与RGCs的凋亡。

Retinal ganglion ceils（RGCs） death and progressive loss is the basic pathology of glaucoma causing visual function damage. RGC death is through the form of apoptosis. After RGC damage, many rea- sons lead to the extraceilular glutamic-acid gathering above the normal level, and causing intracellular Ca2 ＋ increase through the glutamate receptor,and then into a series of cell apoptosis, local glutamate accumulation also causes caspase and TNF alpha increases, commonly involved in RGCs apoptosis.