Hypoxia-ischemia and retinal ganglion cell damage

Charanjit Kaur1, Wallace S Foulds2, Eng-Ang Ling11Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; 2Singapore Eye Research Institute, SingaporeAbstract: Retinal hypoxia is the potentially blinding mechanism underlying a number of sight-threatening...

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Autores principales:	Charanjit Kaur, Wallace S Foulds, Eng-Ang Ling
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2008
Materias:	Ophthalmology RE1-994
Acceso en línea:	https://doaj.org/article/376fbc9b1bf34294a8a9ae2cbe81cf87
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spelling	oai:doaj.org-article:376fbc9b1bf34294a8a9ae2cbe81cf872021-12-02T08:42:51ZHypoxia-ischemia and retinal ganglion cell damage1177-54671177-5483https://doaj.org/article/376fbc9b1bf34294a8a9ae2cbe81cf872008-08-01T00:00:00Zhttp://www.dovepress.com/hypoxia-ischemia-and-retinal-ganglion-cell-damage-a1978https://doaj.org/toc/1177-5467https://doaj.org/toc/1177-5483Charanjit Kaur1, Wallace S Foulds2, Eng-Ang Ling11Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; 2Singapore Eye Research Institute, SingaporeAbstract: Retinal hypoxia is the potentially blinding mechanism underlying a number of sight-threatening disorders including central retinal artery occlusion, ischemic central retinal vein thrombosis, complications of diabetic eye disease and some types of glaucoma. Hypoxia is implicated in loss of retinal ganglion cells (RGCs) occurring in such conditions. RGC death occurs by apoptosis or necrosis. Hypoxia-ischemia induces the expression of hypoxia inducible factor-1&alpha; and its target genes such as vascular endothelial growth factor (VEGF) and nitric oxide synthase (NOS). Increased production of VEGF results in disruption of the blood retinal barrier leading to retinal edema. Enhanced expression of NOS results in increased production of nitric oxide which may be toxic to the cells resulting in their death. Excess glutamate release in hypoxic-ischemic conditions causes excitotoxic damage to the RGCs through activation of ionotropic and metabotropic glutamate receptors. Activation of glutamate receptors is thought to initiate damage in the retina by a cascade of biochemical effects such as neuronal NOS activation and increase in intracellular Ca2+ which has been described as a major contributing factor to RGC loss. Excess production of proinflammatory cytokines also mediates cell damage. Besides the above, free-radicals generated in hypoxic-ischemic conditions result in RGC loss because of an imbalance between antioxidant- and oxidant-generating systems. Although many advances have been made in understanding the mediators and mechanisms of injury, strategies to improve the damage are lacking. Measures to prevent neuronal injury have to be developed.Keywords: retinal hypoxia, retinal ganglion cells, glutamate receptors, neuronal injury, retina Charanjit KaurWallace S FouldsEng-Ang LingDove Medical PressarticleOphthalmologyRE1-994ENClinical Ophthalmology, Vol 2008, Iss Issue 4, Pp 879-889 (2008)
institution	DOAJ
collection	DOAJ
language	EN
topic	Ophthalmology RE1-994
spellingShingle	Ophthalmology RE1-994 Charanjit Kaur Wallace S Foulds Eng-Ang Ling Hypoxia-ischemia and retinal ganglion cell damage
description	Charanjit Kaur1, Wallace S Foulds2, Eng-Ang Ling11Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; 2Singapore Eye Research Institute, SingaporeAbstract: Retinal hypoxia is the potentially blinding mechanism underlying a number of sight-threatening disorders including central retinal artery occlusion, ischemic central retinal vein thrombosis, complications of diabetic eye disease and some types of glaucoma. Hypoxia is implicated in loss of retinal ganglion cells (RGCs) occurring in such conditions. RGC death occurs by apoptosis or necrosis. Hypoxia-ischemia induces the expression of hypoxia inducible factor-1&alpha; and its target genes such as vascular endothelial growth factor (VEGF) and nitric oxide synthase (NOS). Increased production of VEGF results in disruption of the blood retinal barrier leading to retinal edema. Enhanced expression of NOS results in increased production of nitric oxide which may be toxic to the cells resulting in their death. Excess glutamate release in hypoxic-ischemic conditions causes excitotoxic damage to the RGCs through activation of ionotropic and metabotropic glutamate receptors. Activation of glutamate receptors is thought to initiate damage in the retina by a cascade of biochemical effects such as neuronal NOS activation and increase in intracellular Ca2+ which has been described as a major contributing factor to RGC loss. Excess production of proinflammatory cytokines also mediates cell damage. Besides the above, free-radicals generated in hypoxic-ischemic conditions result in RGC loss because of an imbalance between antioxidant- and oxidant-generating systems. Although many advances have been made in understanding the mediators and mechanisms of injury, strategies to improve the damage are lacking. Measures to prevent neuronal injury have to be developed.Keywords: retinal hypoxia, retinal ganglion cells, glutamate receptors, neuronal injury, retina
format	article
author	Charanjit Kaur Wallace S Foulds Eng-Ang Ling
author_facet	Charanjit Kaur Wallace S Foulds Eng-Ang Ling
author_sort	Charanjit Kaur
title	Hypoxia-ischemia and retinal ganglion cell damage
title_short	Hypoxia-ischemia and retinal ganglion cell damage
title_full	Hypoxia-ischemia and retinal ganglion cell damage
title_fullStr	Hypoxia-ischemia and retinal ganglion cell damage
title_full_unstemmed	Hypoxia-ischemia and retinal ganglion cell damage
title_sort	hypoxia-ischemia and retinal ganglion cell damage
publisher	Dove Medical Press
publishDate	2008
url	https://doaj.org/article/376fbc9b1bf34294a8a9ae2cbe81cf87
work_keys_str_mv	AT charanjitkaur hypoxiaischemiaandretinalganglioncelldamage AT wallacesfoulds hypoxiaischemiaandretinalganglioncelldamage AT engangling hypoxiaischemiaandretinalganglioncelldamage
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Hypoxia-ischemia and retinal ganglion cell damage

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