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• W60459021 abstract "The increase of IOP in POAG is due an increased resistance of aqueous outflow through the trabecular meshwork (TM). The exact mechanisms leading to the corresponding changes in the TM are not yet known. We know, however, that all risk factors for arteriosclerosis are also risk factors for an increase in IOP.The association between IOP increase and these factors is relatively weak but nevertheless significant. Similar to the pathogenesis of arteriosclerosis, oxidative stress plays a role in the development of TM damage. Even less is known about the pathogenesis of glaucomatous optic neuropathy (GON). Obviously the risk factors for arteriosclerosis play a role via increasing the IOP. When corrected for IOP, however, these factors only play a minor role. In contrast, factors associated with disturbed autoregulation, in particular a systemic primary vascular dysregulation (PVD), increase the risk for GON. This is best observed in normal tension glaucoma patients. An insufficient autoregulation increases the chance for an unstable ocular perfusion and thereby an unstable oxygen supply. This, in turn, leads to oxidative stress. The concentration of superoxide (O(2)(-)) within the axons of the optic nerve head increases. If neighboring astrocytes are activated, either by mechanical or by ischemic stress, in excess produced nitric oxide (NO) molecules diffuse also into the axons and fuse with oxygen. The resulting peroxynitrat (ONOO(-)) diffuses within the axons towards the retina and the lateral geniculate nucleus and induces apoptosis." @default.
• W60459021 created "2016-06-24" @default.
• W60459021 creator A5000785055 @default.
• W60459021 creator A5042919617 @default.
• W60459021 creator A5066802902 @default.
• W60459021 date "2008-01-31" @default.
• W60459021 modified "2023-09-23" @default.
• W60459021 title "Oxygen and blood flow: players in the pathogenesis of glaucoma." @default.
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• W60459021 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2267728" @default.
• W60459021 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18334938" @default.
• W60459021 hasPublicationYear "2008" @default.
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