Neuroinflammation in Glaucoma and Optic Nerve Damage

被引:71
|
作者
Mac Nair, Caitlin E. [1 ,2 ]
Nickells, Robert W. [1 ]
机构
[1] Univ Wisconsin, Ophthalmol & Visual Sci, Madison, WI 53705 USA
[2] Univ Wisconsin, Cellular & Mol Pathol Grad Program, Madison, WI USA
来源
关键词
TUMOR-NECROSIS-FACTOR; RETINAL GANGLION-CELLS; FACTOR-ALPHA; MOUSE MODEL; TNF-ALPHA; SECONDARY DEGENERATION; EXTRACELLULAR ATP; UP-REGULATION; CRUSH INJURY; MICROGLIAL ACTIVATION;
D O I
10.1016/bs.pmbts.2015.06.010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Glaucoma is a group of optic neuropathies characterized by the degeneration of retinal ganglion cell axons and somas, ultimately preventing light signals in the retina from reaching the brain. Glaucoma is a leading cause of blindness in the world, and treatment options for patients remain limited and minimally efficacious. A number of mechanisms have been linked to glaucomatous pathophysiology. A leading role is now attributed to neuroinflammatory conditions generated by the resident innate immune cells in the optic nerve and retina. Since the eye is immune privileged, the adaptation of these innate immune cells, termed glia, is crucial following trauma. In this chapter, we discuss the mechanisms associated with normal glial function in a healthy eye, and how changes in glial activation can contribute to the process of glaucomatous neurodegeneration in both the optic nerve and retina.
引用
收藏
页码:343 / 363
页数:21
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