Nitric Oxide Synthase in the Human Glaucomatous Optic Nerve Head

Neufeld, Arthur H.; Hernandez, M. Rosario; González, Marı́a José

doi:10.1001/archopht.1997.01100150499009

Cited by 307 publications

(186 citation statements)

References 32 publications

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“…Aberrant nitric oxide synthesis has also been demonstrated within the glaucomatous anterior optic nerve. 78 Neural ischemia could initiate any or all of these apoptotic triggers. Ischemia of the anterior optic nerve results in a blockade of axoplasmic flow, which would prevent normal transport of agents such as growth factors.…”

Section: Ischemia and Neural Damagementioning

confidence: 99%

Ischemic model of optic nerve injury

Cioffi

2006

American Journal of Ophthalmology

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Section: Ischemia and Neural Damagementioning

confidence: 99%

Ischemic model of optic nerve injury

Cioffi

2006

American Journal of Ophthalmology

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“…25 Interestingly, in patients with glaucomatous optic neuropathy, levels of the enzymes cyclooxygenase-1 and nitric oxide synthase, which are involved in the synthesis of eicosanoids and nitric oxide, respectively, and are associated with retinal astrocytes, are elevated in glaucomatous eyes. 26,27 Likewise, in animal models of glaucoma, ganglion cell death is attenuated by treatment with inhibitors of astrocyteassociated nitric oxide synthase. 28 These data support the view that nitric oxide is one toxic factor that is released from astrocytes in glaucoma and damages ganglion cells.…”

Section: Introductionmentioning

confidence: 99%

Optic nerve and neuroprotection strategies

Osborne

Chidlow

Layton

et al. 2004

Eye

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Background Experimental studies have yielded a wealth of information related to the mechanism of ganglion cell death following injury either to the mylinated ganglion cell axon or to the ganglion cell body. However, no suitable animal models exist where injury can be directed to the optic nerve head region, particularly the unmylinated ganglion cell axons. The process of relating the data from the various animal models to many different types of optic neuropathies in man must, therefore, be cautious. Results Extensive studies on the isolated optic nerve have yielded valuable information on the way white matter is affected by ischaemia and how certain types of compounds can attenuate the process. Moreover, there are now persuasive data on how ganglion cell survival is affected when the ocular blood flow is reduced in various animal models. As a consequence, the molecular mechanisms involved in ganglion cell death are fairly well understood and various pharmacological agents have been shown to blunt the process when delivered before or shortly after the insult. Conclusions A battery of agents now exist that can blunt animal ganglion cell death irrespective of whether the insult was to the ganglion cell body or the mylinated axon. Whether this information can be applied for use in patients remains a matter of debate, and major obstacles need to be overcome before the laboratory studies may be applied clinically. These include the delivery of the pharmacological agents to the site of ganglion cell injury and side effects to the patients. Moreover, it is necessary to establish whether effective neuroprotection is only possible when the drug is administered at a defined time after injury to the ganglion cells. This information is essential in order to pursue the idea that a neuroprotective strategy can be applied to a disease like glaucoma, where

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“…They have multiple complex functions, such as inhibiting intermediate proteins that activate caspases. 30 One of the primary regulatory steps in apoptosis is the activation of the tumor suppression protein, p53. This protein functions as a transcription factor that can up-regulate the expression of the pro-apoptotic gene bax and down-regulate the expression of the anti-apoptotic gene Bcl-2.…”

Section: Gene Therapymentioning

confidence: 99%