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. Author manuscript; available in PMC: 2007 Sep 1.
Published in final edited form as: Prog Retin Eye Res. 2006 Sep 7;25(5):490–513. doi: 10.1016/j.preteyeres.2006.07.003

Figure 3.

Figure 3

In addition to neurodegenerative injury induced by intracellular ROS, ROS released from stressed cells into the extracellular milieu may also facilitate secondary degeneration of RGCs. ROS released by neighboring cells may be directly cytotoxic to primarily undamaged RGCs. Alternatively, various consequences of oxidative stress-induced dysfunction of supportive glia may take part in spreading neuronal damage by secondary degeneration of RGCs. By leading to glial dysfunction, oxidative stress-induced glial activation, glial protein oxidation, and AGE/RAGE signaling may all contribute to decreased glial support of RGCs. By stimulating the antigen presenting ability of glial cells, ROS may also be involved in aberrant activation of the immune system, thereby facilitating the progression of glaucomatous neurodegeneration.