Abstract
Retinal ganglion cell (RGC) survival is critical for vision, but these neurons are exquisitely sensitive to insults. In acute diseases such as ischaemic optic neuropathy or optic neuritis, or in chronic diseases such as glaucoma, injury to RGC axons in the optic nerve may lead to rapid RGC death. Retinal ischaemia and retinal artery or vein occlusions directly injure RGC cell bodies in the ganglion cell layer. Enhancing RGC viability (neuroprotection) or RGC function (neuroenhancement) remains a major goal of basic and translational research. In this article we review the many mechanisms that lead from such insults to RGC death in clinically relevant pathological processes, and discuss avenues being pursued to enhance RGC survival in human disease.
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CITATION STYLE
Corredor, R. G., & Goldberg, J. L. (2009). Retinal Ganglion Cell Life and Death – Mechanisms and Implications for Ophthalmology. European Ophthalmic Review, 03(02), 109. https://doi.org/10.17925/eor.2009.03.02.109
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