Department of Glaucoma, Aravind Eye Hospital, Pondicherry, India.
Department of Glaucoma, Wills Eye Hospital, Philadelphia, PA, USA.
Indian J Ophthalmol. 2022 Feb;70(2):380-385. doi: 10.4103/ijo.IJO_1158_21.
Neuroprotective therapies in glaucoma may play a role in preventing ischemia and oxidative damage that results in apoptosis of retinal ganglion cells and optic nerve damage. Although intraocular pressure (IOP) is the only known modifiable risk factor for glaucoma, disease progression commonly occurs despite IOP control, suggesting that factors other than IOP play a role in its pathogenesis and can potentially act as targets for neuroprotection. Factors including mediators of apoptosis, ischemic changes, poor ocular blood flow and neurotoxins have been hypothesized to play a role in glaucoma progression. Neuroprotective targets include glutamate-induced neurotoxicity, nitric oxidase synthetase, neurotropins, calcium channel receptors, free radicals, vascular insufficiency, the rho-kinase pathway, and more. Drugs related to these factors are being evaluated for their role in neuroprotection, although this area of investigation faces several challenges including limited evidence for these agents' efficacy in clinical studies. Additionally, while IOP-lowering therapies are considered neuroprotective as they generally slow the progress of glaucoma progression, they are limited by the extent of their effect beyond IOP control. The aim of this article is to review the current treatment options available for neuroprotection and to explore the drugs in the pipeline.
神经保护疗法在青光眼治疗中可能具有重要作用，可以预防缺血和氧化损伤，从而阻止视网膜神经节细胞凋亡和视神经损伤。虽然眼压（IOP）是青光眼唯一已知的可调节危险因素，但即使控制了 IOP，疾病仍会继续进展，这表明除了 IOP 以外的其他因素在其发病机制中起作用，并可能成为神经保护的靶点。包括凋亡介质、缺血变化、眼血流不良和神经毒素在内的多种因素被认为与青光眼进展有关。神经保护的靶点包括谷氨酸诱导的神经毒性、一氧化氮合酶、神经营养因子、钙通道受体、自由基、血管不足、rho 激酶通路等。与这些因素相关的药物正在评估其神经保护作用，尽管这一研究领域面临着一些挑战，包括这些药物在临床研究中的疗效证据有限。此外，虽然降低眼压的治疗方法被认为具有神经保护作用，因为它们通常可以减缓青光眼进展，但它们受到 IOP 控制以外的作用程度的限制。本文旨在综述现有的神经保护治疗选择，并探讨正在研发中的药物。
