Glaucoma is no longer viewed simply as elevated intraocular pressure (IOP) that damages the optic nerve. In addition to high IOP, evidence is rapidly accumulating that suggests damage to the optic nerve may be initiated or sustained by any number of factors including ischemia, excitotoxicity, neurotrophin insufficiency, peroxynitrite damage or others not yet defined. These different harmful influences then likely act through common final pathways that eventually activate the cellular proteases that accompany neuronal programmed cell death. We believe aberrant immune signal processing may also result in retinal ganglion cell death. We hypothesized that one form of glaucoma may be an autoimmune neuropathy in which an individual's immune system is not only inappropriately regulated, but a cytotoxic effect is rendered by the very system which normally serves to protect it against stress. We propose that the family of proteins termed "heat shock proteins" are critical modulators of both the homeostatic/cytoprotective as well as pathogenic/neurodegenerative arms of the immune system in retinal ganglion cells or glial cells and are thus integral to glaucomatous neurodegeneration.
|Original language||English (US)|
|Number of pages||8|
|Journal||Brain Research Bulletin|
|State||Published - Feb 15 2004|
- Heat shock proteins
- Immune system
ASJC Scopus subject areas