Retinal ganglion cell (RGC) death is the ultimate cause of vision loss in glaucoma. Apoptosis has been thought to be a major form of cell death in various diseases including glaucoma; however, attempts to develop neuroprotective agents that target apoptosis have largely failed. Recent accumulating evidence has shown that non-apoptotic forms of cell death such as necrosis are also regulated by specific molecular machinery, such as those mediated by receptor-interacting protein (RIP) kinases. In this review, we summarize recent advances in our understanding of RIP kinase signaling and its roles in RGC loss. These data suggest that not only apoptosis but also necrosis is involved in RGC death and that combined targeting of these pathways may be an effective strategy for glaucoma.
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