Gossman Cynthia A, Christie John, Webster Mark K, Linn David M, Linn Cindy L
Western Michigan University, Department of Biological Sciences, Kalamazoo, MI 49008.
Curr Pharm Des. 2016;22(14):2178-92. doi: 10.2174/1381612822666160128144747.
Glaucoma is characterized as a neuropathic disease that causes progressive degeneration of retinal ganglion cells (RGCs) in the retina, resulting in irreversible loss of vision. All conventional treatments for glaucoma are focused on reducing intraocular pressure (IOP) in the anterior chamber of the eye. However, these treatments alone are insufficient to halt the progression of the disease. As a result, neuroprotective strategies have been developed that prevent retinal neuron loss and disease progression.
The goal of this review is to summarize and discuss neuroprotective strategies in glaucoma at the level of the retina and the ganglion cell layer instead of treatments targeting IOP. Recent and past neuroprotective therapies used to prevent the loss of retinal ganglion cells, the loss of axons in the optic nerve and the loss of vision and function associated with glaucoma are presented.
Pharmacological approaches have targeted specific receptors, signaling cascades and neurotrophic factors to induce neuroprotection in the retina, while others have focused on the mechanism of cellular loss associated with glaucoma, including excitotoxicity, oxidative stress and apoptotic processes. In addition to neuroprotective pharmacological treatments, stem cell, gene therapy and viral research have demonstrated neuroprotection against the loss of RGCs in glaucomatous conditions.
It is likely that future development for glaucoma treatment will include a combination of these treatments to prevent the pathophysiology of glaucoma.
青光眼是一种神经病变性疾病,可导致视网膜中的视网膜神经节细胞(RGCs)进行性退化,从而导致不可逆的视力丧失。所有传统的青光眼治疗方法都集中于降低眼前房内的眼压(IOP)。然而,仅这些治疗不足以阻止疾病的进展。因此,已开发出神经保护策略来防止视网膜神经元丧失和疾病进展。
本综述的目的是总结和讨论青光眼在视网膜和神经节细胞层水平的神经保护策略,而非针对眼压的治疗方法。介绍了过去和近期用于预防视网膜神经节细胞丧失、视神经轴突丧失以及与青光眼相关的视力和功能丧失的神经保护疗法。
药理学方法已针对特定受体、信号级联反应和神经营养因子来诱导视网膜中的神经保护作用,而其他方法则专注于与青光眼相关的细胞丧失机制,包括兴奋性毒性、氧化应激和凋亡过程。除了神经保护药理学治疗外,干细胞、基因治疗和病毒研究已证明在青光眼病情下对RGCs丧失具有神经保护作用。
青光眼治疗的未来发展可能将包括这些治疗方法的联合应用,以预防青光眼的病理生理过程。