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青光眼的神经保护靶点。

Targets of Neuroprotection in Glaucoma.

机构信息

North Texas Eye Research Institute, University of North Texas Health Science Center , Fort Worth, Texas.

出版信息

J Ocul Pharmacol Ther. 2018 Jan/Feb;34(1-2):85-106. doi: 10.1089/jop.2017.0041. Epub 2017 Aug 18.

Abstract

Progressive neurodegeneration of the optic nerve and the loss of retinal ganglion cells is a hallmark of glaucoma, the leading cause of irreversible blindness worldwide, with primary open-angle glaucoma (POAG) being the most frequent form of glaucoma in the Western world. While some genetic mutations have been identified for some glaucomas, those associated with POAG are limited and for most POAG patients, the etiology is still unclear. Unfortunately, treatment of this neurodegenerative disease and other retinal degenerative diseases is lacking. For POAG, most of the treatments focus on reducing aqueous humor formation, enhancing uveoscleral or conventional outflow, or lowering intraocular pressure through surgical means. These efforts, in some cases, do not always lead to a prevention of vision loss and therefore other strategies are needed to reduce or reverse the progressive neurodegeneration. In this review, we will highlight some of the ocular pharmacological approaches that are being tested to reduce neurodegeneration and provide some form of neuroprotection.

摘要

视神经进行性神经退行性变和视网膜神经节细胞丧失是青光眼的标志,青光眼是全球致盲的主要原因,其中原发性开角型青光眼(POAG)是西方世界最常见的青光眼形式。虽然已经确定了一些青光眼的基因突变,但与 POAG 相关的基因突变有限,对于大多数 POAG 患者,其病因仍不清楚。不幸的是,这种神经退行性疾病和其他视网膜退行性疾病的治疗方法仍很缺乏。对于 POAG,大多数治疗方法主要集中在减少房水形成、增强葡萄膜巩膜或传统流出、或通过手术手段降低眼内压。在某些情况下,这些努力并不总是能预防视力丧失,因此需要其他策略来减少或逆转进行性神经退行性变。在这篇综述中,我们将重点介绍一些正在测试的眼部药物治疗方法,以减少神经退行性变并提供某种形式的神经保护。

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