Elevation of intraocular pressure (IOP) is a major risk factor for neurodegeneration in glaucoma. Glial cells, which play an important role in normal functioning of retinal neurons, are well involved into retinal ganglion cell (RGC) degeneration in experimental glaucoma animal models generated by elevated IOP. In response to elevated IOP, mGluR I is first activated and Kir4.1 channels are subsequently inhibited, which leads to the activation of Müller cells. Müller cell activation is followed by a complex process, including proliferation, release of inflammatory and growth factors (gliosis). Gliosis is further regulated by several factors. Activated Müller cells contribute to RGC degeneration through generating glutamate receptor-mediated excitotoxicity, releasing cytotoxic factors and inducing microglia activation. Elevated IOP activates microglia, and following morphological and functional changes, these cells, as resident immune cells in the retina, show adaptive immune responses, including an enhanced release of pro-inflammatory factors (tumor neurosis factor-α, interleukins, etc.). These ATP and Toll-like receptor-mediated responses are further regulated by heat shock proteins, CD200R, chemokine receptors, and metabotropic purinergic receptors, may aggravate RGC loss. In the optic nerve head, astrogliosis is initiated and regulated by a complex reaction process, including purines, transmitters, chemokines, growth factors and cytokines, which contributes to RGC axon injury through releasing pro-inflammatory factors and changing extracellular matrix in glaucoma. The effects of activated glial cells on RGCs are further modified by the interplay among different types of glial cells. This review is concluded by presenting an in-depth discussion of possible research directions in this field in the future.

眼内压 (IOP) 升高是青光眼神经变性的主要危险因素。在视网膜神经元的正常功能中发挥重要作用的神经胶质细胞很好地参与了眼压升高产生的实验性青光眼动物模型中的视网膜神经节细胞 (RGC) 变性。响应升高的 IOP，首先激活 mGluR I，随后抑制 Kir4.1 通道，从而激活 Müller 细胞。Müller 细胞激活之后是一个复杂的过程，包括增殖、炎症和生长因子的释放（神经胶质增生）。神经胶质增生进一步受几个因素的调节。激活的 Müller 细胞通过产生谷氨酸受体介导的兴奋性毒性、释放细胞毒性因子和诱导小胶质细胞活化来促进 RGC 退化。眼压升高会激活小胶质细胞，随着形态和功能的变化，这些细胞作为视网膜中的常驻免疫细胞，表现出适应性免疫反应，包括促炎因子（肿瘤神经症因子-α、白细胞介素等）的释放增强。这些 ATP 和 Toll 样受体介导的反应进一步受到热休克蛋白、CD200R、趋化因子受体和代谢性嘌呤能受体的调节，可能会加剧 RGC 损失。在视神经乳头中，星形胶质细胞增生是由一个复杂的反应过程启动和调节的，包括嘌呤、递质、趋化因子、生长因子和细胞因子，它通过释放促炎因子和改变青光眼中的细胞外基质来促进 RGC 轴突损伤。不同类型神经胶质细胞之间的相互作用进一步改变了激活的神经胶质细胞对 RGC 的影响。这篇综述最后对该领域未来可能的研究方向进行了深入讨论。