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Magnesium acethyltaurate as a potential agent for retinal and optic nerve protection in glaucoma

机译:乙基牛磺酸镁可作为青光眼视网膜和视神经保护的潜在药物

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Glaucoma is the second leading cause of irreversible vision impairment affecting more than 70 million people worldwide with approximately 10% suffering from glaucoma-related bilateral blind (Quigley and Broman, 2006). It is a multi-factorial disease that is characterized by optic nerve damage and visual field loss. Progressive loss of retinal ganglion cells (RGCs) resulting in visual field deficits is the hallmark of glaucoma. Sever-al etiological factors seem to be involved in its pathophysiology, however the precise mechanisms leading to its development remain unclear. Some of the widely described factors that contribute to RGC loss include axonal transport failure, neurotrophic factor depletion, excitotoxicity, mitochon-drial dysfunction, activation of intrinsic and extrinsic apoptotic cascade and oxidative stress (Agarwal et al., 2009). The basic mechanisms that contribute to RGC degeneration in glaucoma are presented in Figure 1. Current treatment strategies for glaucoma are limited to the reduction of intraocular pressure (IOP); however, it is clear now that the disease pro-gression may continue despite effective IOP lowering. Search for newer modalities has led to emergence of significant data from experimental re-search suggesting potentially new neuroprotective strategies that may add to the arsenal of existing antiglaucoma agents (Vasudevan et al., 2011).
机译:青光眼是造成不可逆视力障碍的第二个主要原因,影响了全世界超过7000万人,其中约10%患有青光眼相关的双侧盲(Quigley和Broman,2006)。它是一种多因素疾病,以视神经损害和视野丧失为特征。视网膜神经节细胞(RGCs)的逐渐丧失导致视野缺损是青光眼的标志。几个病因似乎与它的病理生理有关,但是导致其发展的确切机制仍不清楚。导致RGC丧失的一些广为人知的因素包括轴突运输失败,神经营养因子耗竭,兴奋性毒性,线粒体-干细胞功能障碍,内在和外在凋亡级联反应的激活以及氧化应激(Agarwal等,2009)。图1显示了导致青光眼RGC变性的基本机制。目前的青光眼治疗策略仅限于降低眼内压(IOP);然而,现在很明显,尽管有效降低了眼压,疾病的进展仍可能继续。对较新形式的寻找已导致来自实验研究的大量数据的出现,表明潜在的新神经保护策略可能会增加现有抗青光眼药物的药库(Vasudevan等人,2011)。

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