You Mengling, Rong Rong, Zeng Zhou, Xia Xiaobo, Ji Dan
Department of Ophthalmology, Xiangya Hospital, Central South University, Changsha, China.
Hunan Key Laboratory of Ophthalmology, Changsha, China.
Front Aging Neurosci. 2021 Apr 6;13:643685. doi: 10.3389/fnagi.2021.643685. eCollection 2021.
The death of retinal ganglion cells (RGCs) is a key factor in the pathophysiology of all types of glaucoma, but the mechanism of pathogenesis of glaucoma remains unclear. RGCs are a group of central nervous system (CNS) neurons whose soma are in the inner retina. The axons of RGCs form the optic nerve and converge at the optic chiasma; from there, they project to the visual cortex the lateral geniculate nucleus (LGN). In recent years, there has been increasing interest in the dysfunction and death of CNS and retinal neurons caused by transneuronal degeneration of RGCs, and the view that glaucoma is a widespread neurodegenerative disease involving CNS damage appears more and more frequently in the literature. In this review, we summarize the current knowledge of LGN and visual cortex neuron damage in glaucoma and possible mechanisms behind the damage. This review presents an updated and expanded view of neuronal damage in glaucoma, and reveals new and potential targets for neuroprotection and treatment.
视网膜神经节细胞(RGCs)的死亡是所有类型青光眼病理生理学的关键因素,但青光眼的发病机制仍不清楚。RGCs是一组中枢神经系统(CNS)神经元,其胞体位于视网膜内层。RGCs的轴突形成视神经并在视交叉处汇聚;从那里,它们投射到视觉皮层和外侧膝状体核(LGN)。近年来,由RGCs跨神经元变性引起的中枢神经系统和视网膜神经元功能障碍及死亡越来越受到关注,并且青光眼是一种涉及中枢神经系统损伤的广泛神经退行性疾病的观点在文献中越来越频繁地出现。在本综述中,我们总结了目前关于青光眼中外侧膝状体核和视觉皮层神经元损伤的知识以及损伤背后的可能机制。本综述提出了关于青光眼神经元损伤的更新和扩展观点,并揭示了神经保护和治疗的新的潜在靶点。