The molecular basis of retinal ganglion cell death in glaucoma
The molecular basis of retinal ganglion cell death in glaucoma
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DOI：
10.1016/j.preteyeres.2011.11.002
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发表时间：
2012-03-01
影响因子：
17.8
通讯作者：
Di Polo, Adriana
中科院分区：
文献类型：
--
作者：
Almasieh, Mohammadali;Wilson, Ariel M.;Di Polo, Adriana
青光眼是一组以进行性视神经变性为特征的疾病，可导致视野丧失和不可逆性失明。所有形式青光眼病理生理学的一个关键因素是视网膜神经节细胞（RGC）的死亡，RGC 是一群中枢神经系统神经元，其体细胞位于视网膜内部，轴突位于视神经。延迟或阻止 RGC 损失的策略已被认为可能有益于保留青光眼患者的视力；然而，这些方法的成功取决于对导致 RGC 功能障碍和死亡的机制的深入了解。近年来，来自急性和慢性视神经损伤以及实验性青光眼动物模型的 RGC 死亡分子基础的有价值信息呈指数级增长。新出现的情况很复杂，并指出多种分子信号（单独或协同作用）会促进 RGC 死亡。这些包括：轴突运输失败、神经营养因子剥夺、有毒前神经营养蛋白、内在和外在细胞凋亡信号的激活、线粒体功能障碍、兴奋性毒性损伤、氧化应激、反应性神经胶质细胞行为不当和突触连接丧失。总的来说，这项工作极大地更新和扩展了我们对 RGC 如何在青光眼中死亡的看法，并揭示了新的、潜在的神经保护靶点。 (C) 2011 年，爱思唯尔有限公司出版。
Glaucoma is a group of diseases characterized by progressive optic nerve degeneration that results in visual field loss and irreversible blindness. A crucial element in the pathophysiology of all forms of glaucoma is the death of retinal ganglion cells (RGCs), a population of CNS neurons with their soma in the inner retina and axons in the optic nerve. Strategies that delay or halt RGC loss have been recognized as potentially beneficial to preserve vision in glaucoma; however, the success of these approaches depends on an in-depth understanding of the mechanisms that lead to RGC dysfunction and death. In recent years, there has been an exponential increase in valuable information regarding the molecular basis of RGC death stemming from animal models of acute and chronic optic nerve injury as well as experimental glaucoma. The emerging landscape is complex and points at a variety of molecular signals - acting alone or in cooperation - to promote RGC death. These include: axonal transport failure, neurotrophic factor deprivation, toxic pro-neurotrophins, activation of intrinsic and extrinsic apoptotic signals, mitochondrial dysfunction, excitotoxic damage, oxidative stress, misbehaving reactive glia and loss of synaptic connectivity. Collectively, this body of work has considerably updated and expanded our view of how RGCs might die in glaucoma and has revealed novel, potential targets for neuroprotection. (C) 2011 Published by Elsevier Ltd.