Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-gu, Seoul, 06351, South Korea.
Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-Ro, Gangnam-gu, Seoul, 06351, South Korea.
Prog Retin Eye Res. 2020 Jul;77:100840. doi: 10.1016/j.preteyeres.2020.100840. Epub 2020 Jan 23.
Neuroretinal rim thinning (NRR) is a characteristic glaucomatous optic disc change. However, the precise mechanism of the rim thinning has not been completely elucidated. This review focuses on the structural role of the glioarchitecture in the formation of the glaucomatous NRR thinning. The NRR is a glia-framed structure, with honeycomb geometry and mechanically reinforced astrocyte processes along the transverse plane. When neural damage selectively involves the neuron and spares the glia, the gross structure of the tissue is preserved. The disorganization and loss of the glioarchitecture are the two hallmarks of optic nerve head (ONH) remodeling in glaucoma that leads to the thinning of NRR tissue upon axonal loss. This is in contrast to most non-glaucomatous optic neuropathies with optic disc pallor where hypertrophy of the glioarchitecture is associated with the seemingly absent optic disc cupping. Arteritic anterior ischemic optic neuropathy is an exception where pan-necrosis of ONH tissue leads to NRR thinning. Milder ischemia indicates selective neuronal loss that spares glia in non-arteritic anterior ischemic optic neuropathy. The biological reason is the heterogeneous glial response determined by the site, type, and severity of the injury. The neuroglial interpretation explains how the cellular changes underlie the clinical findings. Updated understandings on glial responses illustrate the mechanical, microenvironmental, and microglial modulation of activated astrocytes in glaucoma. Findings relevant to the possible mechanism of the astrocyte death in advanced glaucoma are also emerging. Ultimately, a better understanding of glaucomatous glial response may lead to glia-targeting neuroprotection in the future.
神经视网膜边缘变薄（NRR）是青光眼特征性的视神经盘改变。然而，边缘变薄的确切机制尚未完全阐明。本综述重点关注神经胶质细胞结构在青光眼 NRR 变薄形成中的结构作用。NRR 是一种由神经胶质细胞构成的框架结构，具有蜂窝状几何形状和沿横向平面增强的星形胶质细胞过程。当神经损伤选择性地累及神经元而保留神经胶质细胞时，组织的大体结构得以保留。神经胶质细胞结构的紊乱和丧失是青光眼视神经头（ONH）重塑的两个标志，导致轴突丢失时 NRR 组织变薄。这与大多数非青光眼视神经病变形成的视神经盘苍白形成对比，后者与视神经盘杯状变似乎不存在相关的神经胶质细胞肥大。动脉炎性前部缺血性视神经病变是一个例外，ONH 组织的全坏死导致 NRR 变薄。更温和的缺血表明选择性神经元丢失，在非动脉炎性前部缺血性视神经病变中保留神经胶质细胞。生物学原因是由损伤的部位、类型和严重程度决定的异质神经胶质反应。神经胶质细胞的解释说明了细胞变化如何构成临床发现的基础。关于神经胶质细胞反应的最新认识说明了机械、微环境和小胶质细胞对激活星形胶质细胞的调节在青光眼发病机制中的作用。关于晚期青光眼星形胶质细胞死亡的可能机制的研究结果也在不断出现。最终，对青光眼神经胶质细胞反应的更好理解可能会导致未来针对神经胶质细胞的神经保护。
