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- W65040972 endingPage "425" @default.
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- W65040972 abstract "Publisher Summary Despite intensive research efforts over the past decades, the molecular events that cause damage to retinal ganglion cells (RGC) and their axons in primary open angle glaucoma (POAG) have not been substantially clarified. There is evidence though that intraocular pressure (IOP) plays a critical role, as an IOP that is too high for the health of the optic nerve axons has been identified as the most critical risk factor for glaucomatous RGC damage in several prospective, randomized, multicenter clinical studies. IOP is generated in the trabecular meshwork (TM) outflow pathways, which show an abnormally high resistance for aqueous humor outflow in POAG. As of today, there is uncertainty on the nature of the molecular changes that lead to an increase in intraocular pressure (IOP) in POAG. This chapter focuses on the data that are currently available on the function of all of these proteins as related to POAG. It is the strong belief that a more complete understanding of these proteins will substantially help to elucidate the molecular mechanisms that govern aqueous humor outflow through the TM and the pathogenetic mechanisms of POAG." @default.
- W65040972 created "2016-06-24" @default.
- W65040972 creator A5070484493 @default.
- W65040972 date "2008-01-01" @default.
- W65040972 modified "2023-09-26" @default.
- W65040972 title "Chapter 12 Molecular Approaches to Glaucoma" @default.
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