Optic nerve head structure in glaucoma: astrocytes as mediators of axonal damage
Optic nerve head structure in glaucoma: astrocytes as mediators of axonal damage
复制标题
DOI：
10.1038/eye.2000.128
复制
发表时间：
2000-06-01
期刊：
影响因子：
3.9
通讯作者：
Morgan, JE
中科院分区：
文献类型：
--
作者：
Morgan, JE
眼内压（IOP）升高被认为是视盘发生青光眼拔罐的主要危险因素。它通过增加视神经乳头筛板的机械力来破坏视网膜神经节细胞轴突的功能的假设已得到相当多的实验支持。然而，许多青光眼患者即使眼压保持在正常范围内也会进行性拔罐，这表明机械压迫不太可能是视神经损伤的唯一原因。临床研究强调了其他因素（例如视神经乳头缺血）在产生视盘盖的过程中的作用。了解青光眼视神经乳头功能障碍的突出问题之一是阐明可以整合 IOP 和缺血的影响以产生所见特征性变化的途径。本综述考虑了视神经乳头星形胶质细胞在轴突损伤引发中可能发挥的作用，基于这些细胞对机械或缺血因素敏感并且对于维持视网膜神经节生理机能很重要的假设。它讨论了它们在筛板结构重塑中的作用以及这可能对轴突功能的影响。最近的证据表明，星形胶质细胞活性的调节，例如通过减少一氧化氮的产生，可以预防高眼压症中的视网膜神经节细胞死亡。星形胶质细胞-轴突相互作用在青光眼性视神经病变的发展中很重要，这一可能性表明了与眼压控制无关的新的治疗干预途径，这将防止青光眼中视网膜神经节细胞死亡。
Increased intraocular pressure (IOP) is recognised as the principal risk factor for the development of glaucomatous cupping of the optic disc. The hypothesis that it disrupts the function of retinal ganglion cell axons by increasing mechanical forces on the lamina cribrosa of the optic nerve head has received considerable experimental support. However, many patients with glaucoma will have progressive cupping even though the IOPs remain within the normal range, suggesting that mechanical compression is unlikely to be the sole cause of optic nerve damage. Clinical studies have emphasised the role of other factors, such as optic nerve head ischaemia, in generating optic disc copping. One of the outstanding problems in understanding optic nerve head dysfunction in glaucoma has been the elucidation of the pathways that could integrate the effects of IOP and ischaemia to generate the characteristic changes seen. This review considers the role that optic nerve head astrocytes might play in the initiation of axon damage, based on the hypothesis that these cells are sensitive to mechanical or ischaemic factors and are important for the maintenance of retinal ganglion physiology. It discusses their role in the remodelling of the structure of the lamina cribrosa and the effect that this might have on axon function. Recent evidence has shown that the modulation of astrocyte activity, for example by the reduction of the production of nitric oxide, may prevent retinal ganglion cell death in ocular hypertension. The possibility that astrocyte-axon interactions are important in the development of glaucomatous optic neuropathy suggests new avenues of therapeutic intervention, not related to the control of IOP, that would prevent retinal ganglion cell death in glaucoma.