From ocular hypertension to ganglion cell death: a theoretical sequence of events leading to glaucoma
From ocular hypertension to ganglion cell death: a theoretical sequence of events leading to glaucoma
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DOI：
10.3129/canjophthalmol.i07-036
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发表时间：
2007-04-01
影响因子：
4.2
通讯作者：
Nickells, Robert W.
中科院分区：
文献类型：
--
作者：
Nickells, Robert W.
有大量证据表明，高眼压是青光眼的关键危险因素。然而，即使进行了详尽的研究，人们对将高眼压转化为视网膜神经节细胞死亡过程的病理事件仍知之甚少。新的研究，特别是在青光眼大鼠和小鼠模型上的研究，帮助阐明了一些与青光眼发病相关的重要事件。本文总结了5个阶段的假说，即高眼压引起视神经头神经胶质细胞的有害变化(阶段1)，激活神经节细胞轴突的自主自毁(阶段2)，导致视网膜神经节细胞SoMAS失去神经营养支持和细胞凋亡性死亡(阶段3)。在神经节细胞死亡的最初波中，死亡的细胞可能在涉及谷氨酸暴露的次级变性波中对邻近细胞产生不利影响(阶段4)。随着神经节细胞结构在细胞死亡的过程中消失，胶质细胞再次参与其中，但这次是用神经胶质疤痕来取代丢失的神经组织(阶段5)。
There is substantial evidence that elevated intraocular pressure (IOP) is a critical risk factor for glaucoma. Even with exhaustive investigation, however, there is still little understanding of the pathologic events that translate increased IOP into the process of retinal ganglion cell death. New studies, particularly in rat and mouse models of glaucoma, have helped elucidate some of the important events associated with the initiation of glaucoma. This review summarizes a 5-stage series hypothesizing that elevated IOP causes deleterious changes to glia in the optic nerve head (stage 1), which activate the autonomous self-destruction of ganglion cell axons (stage 2), leading to the loss of neurotrophic support and apoptotic death of ganglion cell somas in the retina (stage 3). In the initial wave of ganglion cell death, dying cells may, adversely affect their neighbouring cells in a wave of secondary degeneration involving glutamate exposure (stage 4). As ganglion cell structures disappear through the processes of cell death, glia are again involved, but this time to replace the lost neural tissue with a glial scar (stage 5).