Mechanisms of retinal ganglion cell injury and defense in glaucoma

被引:176
|
作者
Qu, Juan [1 ]
Wang, Danyi [1 ]
Grosskreutz, Cynthia L. [1 ]
机构
[1] Harvard Univ, Sch Med, Dept Ophthalmol, Howe Lab Ophthalmol,Massachusetts Eye & Ear Infir, Boston, MA 02114 USA
关键词
apoptosis; neuroprotection; caspase; calcineurin; calpain; NITRIC-OXIDE SYNTHASE; NECROSIS-FACTOR-ALPHA; OPTIC-NERVE DAMAGE; ELEVATED INTRAOCULAR-PRESSURE; CHRONIC OCULAR HYPERTENSION; EARLY GENE-EXPRESSION; OPEN-ANGLE GLAUCOMA; LONG-TERM SURVIVAL; NEUROTROPHIC FACTOR; ADULT-RATS;
D O I
10.1016/j.exer.2010.04.002
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Glaucoma is a disease in which retinal ganglion cells (RGCs) die leading ultimately to blindness. Over the past decade and a half, information has begun to emerge regarding specific molecular responses of the retina to conditions of elevated intraocular pressure (IOP). It is now clear that the state of the RGC in glaucoma depends on a balance of pro-survival and pro-death pathways in the retina and details of these responses are still being worked out. In this review, we will discuss the evidence supporting the involvement of specific apoptotic cascades as well as the insults that trigger RGC apoptosis. In addition, we will present evidence supporting the existence of endogenous protective mechanisms as well as exogenous neuroprotective strategies. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:48 / 53
页数:6
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