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Abstract #57466 Published in IGR 16-2
Retinal ganglion cell death is triggered by paraptosis via reactive oxygen species production: A brief literature review presenting a novel hypothesis in glaucoma pathology
Xu K; Zhang H; Zhao J; Zhu X; Wang Y; Wu RMolecular medicine reports 2014; 10: 1179-1183
Accumulative evidence has indicated that apoptosis is the common pathway for retinal ganglion cell (RGC) death and that autophagy promotes survival of RGCs in glaucoma. In the present review, it was hypothesized that the progressive death of RGCs in glaucoma involves another novel non‑apoptotic programmed cell death, known as 'paraptosis', in the early stages of glaucoma. Paraptosis may be accompanied by apoptosis and/or autophagy in the moderate and severe stages. The secondary hypothesis suggests that paraptosis in glaucomatous RGCs may be triggered by damage to cellular mitochondria, and is associated with mitochondria-derived reactive oxygen species (ROS). Our preliminary laboratory studies, using transmission electron microscopy, provided evidence that supports the primary hypothesis. The secondary hypothesis is currently under investigation. These two hypotheses provide a novel way to investigate the mechanisms of cell death in glaucomatous RGCs and targeting paraptosis may be a promising strategy for RGC-protecting drug discovery.
Full article
Classification:
3.9 Pathophysiology (Part of: 3 Laboratory methods)
11.8 Neuroprotection (Part of: 11 Medical treatment)
3.6 Cellular biology (Part of: 3 Laboratory methods)
3.7 Biochemistry (Part of: 3 Laboratory methods)
