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视网膜神经节细胞(RGCs)的过度凋亡是青光眼病理改变的基础。Mller细胞作为视网膜的主要神经胶质细胞,对于维持神经元的完整性、代谢、内环境稳态以及信号转导等均具有重要的作用。随着对Mller细胞研究的逐渐深入,发现Mller细胞不仅参与了青光眼性RGCs的凋亡机制,而且还参与了RGCs的代偿性保护机制。那么Mller细胞是如何对RGCs起作用,它又是通过什么机制参与青光眼引起的RGCs凋亡以及代偿性保护作用呢?就这些问题的最新研究进展进行综述。
The excessive apoptosis of retinal ganglion cells (RGCs) is the basis of pathological changes in glaucoma. Mäller cells, as the main glial cells of the retina, play an important role in maintaining neuronal integrity, metabolism, homeostasis and signal transduction. With the deepening of researches on Mller cells, Mller cells were found not only involved in the apoptosis mechanism of glaucoma RGCs, but also involved in the compensatory mechanism of RGCs. So how does M? Ller cells play a role in RGCs, and through which mechanisms participate in the apoptosis of RGCs induced by glaucoma and the compensatory protective effect? The recent research progress on these problems are reviewed.