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Current concepts in the pathophysiology of glaucoma.

Agarwal R, Gupta SK, Agarwal P, Saxena R, Agrawal SS - Indian J Ophthalmol (2009 Jul-Aug)

Bottom Line: Extensive investigations into the pathophysiology of glaucoma now reveal the role of multiple factors in the development of retinal ganglion cell death.A better understanding of the pathophysiological mechanisms involved in the onset and progression of glaucomatous optic neuropathy is crucial in the development of better therapeutic options.The literature available in the National Medical Library and online Pubmed search engine was used for literature review.

View Article: PubMed Central - PubMed

Affiliation: Department of Ocular Pharmacology, Delhi Institute of Pharmaceutical Sciences and Research, New Delhi, India.

ABSTRACT
Glaucoma, the second leading cause of blindness, is characterized by changes in the optic disc and visual field defects. The elevated intraocular pressure was considered the prime factor responsible for the glaucomatous optic neuropathy involving death of retinal ganglion cells and their axons. Extensive investigations into the pathophysiology of glaucoma now reveal the role of multiple factors in the development of retinal ganglion cell death. A better understanding of the pathophysiological mechanisms involved in the onset and progression of glaucomatous optic neuropathy is crucial in the development of better therapeutic options. This review is an effort to summarize the current concepts in the pathophysiology of glaucoma so that newer therapeutic targets can be recognized. The literature available in the National Medical Library and online Pubmed search engine was used for literature review.

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Mechanisms involved in glaucomatous RGC apoptosis secondary to elevated IOP. TNF-A - Tumor necrosis factor-alpha, MMP - Matrix metalloproteinase, NOS-2 - Nitric oxide synthase-2
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Figure 0001: Mechanisms involved in glaucomatous RGC apoptosis secondary to elevated IOP. TNF-A - Tumor necrosis factor-alpha, MMP - Matrix metalloproteinase, NOS-2 - Nitric oxide synthase-2

Mentions: Nakazawa et al., have now demonstrated rapid upregulation of TNF-A in rats with experimentally induced elevated IOP and this was followed sequentially by microglial activation, loss of optic nerve oligodendrocytes, and delayed loss of RGCs.[46] An upregulation of TNF-A in the astrocytes was also detected in human glaucomatous optic nerve head and this expression was found to parallel the progression of neurodegeneration. TNF-A stimulation seems to contribute to neuronal damage by both a direct effect on the axons of the RGCs and by inducing nitric oxide synthase (NOS)-2 in astrocytes.[47] A summary of mechanisms involved in RGC apoptosis secondary to elevated IOP is presented in Fig. 1.


Current concepts in the pathophysiology of glaucoma.

Agarwal R, Gupta SK, Agarwal P, Saxena R, Agrawal SS - Indian J Ophthalmol (2009 Jul-Aug)

Mechanisms involved in glaucomatous RGC apoptosis secondary to elevated IOP. TNF-A - Tumor necrosis factor-alpha, MMP - Matrix metalloproteinase, NOS-2 - Nitric oxide synthase-2
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2712693&req=5

Figure 0001: Mechanisms involved in glaucomatous RGC apoptosis secondary to elevated IOP. TNF-A - Tumor necrosis factor-alpha, MMP - Matrix metalloproteinase, NOS-2 - Nitric oxide synthase-2
Mentions: Nakazawa et al., have now demonstrated rapid upregulation of TNF-A in rats with experimentally induced elevated IOP and this was followed sequentially by microglial activation, loss of optic nerve oligodendrocytes, and delayed loss of RGCs.[46] An upregulation of TNF-A in the astrocytes was also detected in human glaucomatous optic nerve head and this expression was found to parallel the progression of neurodegeneration. TNF-A stimulation seems to contribute to neuronal damage by both a direct effect on the axons of the RGCs and by inducing nitric oxide synthase (NOS)-2 in astrocytes.[47] A summary of mechanisms involved in RGC apoptosis secondary to elevated IOP is presented in Fig. 1.

Bottom Line: Extensive investigations into the pathophysiology of glaucoma now reveal the role of multiple factors in the development of retinal ganglion cell death.A better understanding of the pathophysiological mechanisms involved in the onset and progression of glaucomatous optic neuropathy is crucial in the development of better therapeutic options.The literature available in the National Medical Library and online Pubmed search engine was used for literature review.

View Article: PubMed Central - PubMed

Affiliation: Department of Ocular Pharmacology, Delhi Institute of Pharmaceutical Sciences and Research, New Delhi, India.

ABSTRACT
Glaucoma, the second leading cause of blindness, is characterized by changes in the optic disc and visual field defects. The elevated intraocular pressure was considered the prime factor responsible for the glaucomatous optic neuropathy involving death of retinal ganglion cells and their axons. Extensive investigations into the pathophysiology of glaucoma now reveal the role of multiple factors in the development of retinal ganglion cell death. A better understanding of the pathophysiological mechanisms involved in the onset and progression of glaucomatous optic neuropathy is crucial in the development of better therapeutic options. This review is an effort to summarize the current concepts in the pathophysiology of glaucoma so that newer therapeutic targets can be recognized. The literature available in the National Medical Library and online Pubmed search engine was used for literature review.

Show MeSH
Related in: MedlinePlus