Retinal ganglion cell death is the final common pathway of virtually all diseases of the optic nerve, including glaucomatous optic neuropathy. In recent years it has been shown that retinal ganglion cells die after axonal injury via a programmed cell death process called apoptosis. The dynamics of retinal ganglion cell death reflect the timing and degree of the axonal injury, rather than its nature. For example, whether mediated by ischemia (corresponding to abnormalities of peripapillary circulation) or compression (e.g., changes in retrograde transport caused by increased intraocular pressure), the end result is a series of changes at the level of the axon, which subsequently affect the retinal ganglion cell body. Our studies on neuroprotection of retinal ganglion cells have focused on general mechanisms applicable to axonal injuries. By dissecting the pathways by which retinal ganglion cells die in these situations, strategies for protection may become manifest. We and others have found that production of certain reactive oxygen species is a necessary step for neuronal death after neurotrophin deprivation. In response, cells invoke compensatory mechanisms to maintain survival in the face of this attack. We have studied the transcriptional regulation of one candidate compensatory gene and discuss it as a model for gene-based approaches to neuroprotective therapy for glaucomatous optic neuropathy. By approaching the problem of therapy from this point of view, it may become possible to prevent irreversible glaucomatous optic nerve changes by inducing endogenous cell-rescue mechanisms and, thus, with the retinal ganglion cells’ own defense mechanisms, to prevent its death.
Survey of Ophthalmology – Elsevier
Published: Jun 1, 1999
It’s your single place to instantly
discover and read the research
that matters to you.
Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.
All for just $49/month
Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly
Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.
Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.
Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.
All the latest content is available, no embargo periods.
“Hi guys, I cannot tell you how much I love this resource. Incredible. I really believe you've hit the nail on the head with this site in regards to solving the research-purchase issue.”Daniel C.
“Whoa! It’s like Spotify but for academic articles.”@Phil_Robichaud
“I must say, @deepdyve is a fabulous solution to the independent researcher's problem of #access to #information.”@deepthiw
“My last article couldn't be possible without the platform @deepdyve that makes journal papers cheaper.”@JoseServera