青光眼疾病中视网膜胶质细胞的作用

青光眼是一种视网膜视神经的退行性病变,以视网膜神经节细胞(RGCs)的凋亡为基本病理基础,但其凋亡的具体机制尚未完全阐明.目前,大量在体及体外研究发现,视网膜胶质细胞,如Müller胶质细胞、星形胶质细胞和小胶质细胞与青光眼的发生和发展,特别是RGCs的损伤密切相关.胶质细胞上存在众多神经递质受体、离子通道、表面标志物及效应分子,同时也可释放活性因子,因此胶质细胞除了传统认为的具有对神经元的支持营养作用外,还积极参与神经元之间的信息传递过程.在青光眼条件下,胶质细胞可被激活并产生许多生理、生化及形态学改变,一方面可释放神经保护因子,启动神经保护程序;另一方面在胶质细胞过度激活时也会影响其正常生理功能或释放有害因子,加重视网膜神经元的损伤.这2种作用在青光眼中常常并存,但目前这些作用的潜在机制和相关信号通路尚不十分清楚,因而青光眼神经元损伤后胶质细胞是如何重建或进一步破坏神经元功能需要进行更多的研究.本文对视网膜Müller细胞、星形胶质细胞及小胶质细胞的基本生理特征,以及在青光眼病理过程中各自的功能变化进行综述.

Current researches on effects of retinal neuroglial cells in glaucoma

Glaucoma is a degenerative disease of the retina and the optic nerve.The apoptosis of retinal ganglion cells is the pathological basis of glaucoma,but its mechanism has not been fully elucidated.Currently,a large number of studies in vivo and in vitro have demonstrated that retinal glial cells (including Müller cells,astrocytes and microglial cells) are closely related to the development of glaucoma.Retinal glial cells not only release active factors but also express various neurotransmitter receptors,ion channels,surface markers and effector molecules.Therefore,they are actively involved in neuronal information transmission in addition to the traditional view of the role of nutritional support for neurons.In glaucoma,retinal glial cells are activated to undergo a great number of changes in physiology,biochemistry and morphological features.These activated cells initiate different signaling cascades that may serve as a protective role.Meanwhile,they may release toxic factors to start or aggravate the damaging effects on retinal neurons.Usually,both effects occur in glaucoma in parallel,but the underlying mechanisms and signaling pathways are still not clear.More research is needed to understand that how the retinal glial cells are able to rebuild the neuronal function after injury or to promote the neurodamage.With all these unresolved issues in mind,the progress in the study of the mechanism of Müller glial cells,microglial cells and astrocytes participating in the glaucomatous disease were reviewed.