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Oxygen and blood flow: players in the pathogenesis of glaucoma
PURPOSE: The increase of IOP in POAG is due an increased resistance of aqueous outflow through the trabecular meshwork (TM). METHODS: 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 fact...
Autores principales: | , , |
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Formato: | Texto |
Lenguaje: | English |
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Molecular Vision
2008
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267728/ https://www.ncbi.nlm.nih.gov/pubmed/18334938 |
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author | Mozaffarieh, Maneli Grieshaber, Matthias C. Flammer, Josef |
author_facet | Mozaffarieh, Maneli Grieshaber, Matthias C. Flammer, Josef |
author_sort | Mozaffarieh, Maneli |
collection | PubMed |
description | PURPOSE: The increase of IOP in POAG is due an increased resistance of aqueous outflow through the trabecular meshwork (TM). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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. |
format | Text |
id | pubmed-2267728 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | Molecular Vision |
record_format | MEDLINE/PubMed |
spelling | pubmed-22677282008-03-20 Oxygen and blood flow: players in the pathogenesis of glaucoma Mozaffarieh, Maneli Grieshaber, Matthias C. Flammer, Josef Mol Vis Review PURPOSE: The increase of IOP in POAG is due an increased resistance of aqueous outflow through the trabecular meshwork (TM). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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. Molecular Vision 2008-01-31 /pmc/articles/PMC2267728/ /pubmed/18334938 Text en Copyright © 2008 Molecular Vision. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Mozaffarieh, Maneli Grieshaber, Matthias C. Flammer, Josef Oxygen and blood flow: players in the pathogenesis of glaucoma |
title | Oxygen and blood flow: players in the pathogenesis of glaucoma |
title_full | Oxygen and blood flow: players in the pathogenesis of glaucoma |
title_fullStr | Oxygen and blood flow: players in the pathogenesis of glaucoma |
title_full_unstemmed | Oxygen and blood flow: players in the pathogenesis of glaucoma |
title_short | Oxygen and blood flow: players in the pathogenesis of glaucoma |
title_sort | oxygen and blood flow: players in the pathogenesis of glaucoma |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2267728/ https://www.ncbi.nlm.nih.gov/pubmed/18334938 |
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