Protocol for Corticosteroid-Induced Ocular Hypertension and Glaucomatous Optic Neuropathy in Rodents
- Authors: Najam A. Sharif1, Saima Chaudhry2
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View Affiliations Hide Affiliations1 Vice President and Head of Research & Development Nanoscope Therapeutics Inc., 2777 N. Stemmons Fwy, Suite 1102, Dallas, TX 75207, USA 2 Univ N. Texas at Arlington, 701 S Nedderman Dr, Arlington, TX-76019, USA
- Source: Research Protocols for Ophthalmic Disease Mechanisms and Therapeutics: Glaucoma - Ocular Hypertension , pp 327-336
- Publication Date: August 2025
- Language: English
Protocol for Corticosteroid-Induced Ocular Hypertension and Glaucomatous Optic Neuropathy in Rodents, Page 1 of 1
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Many forms of glaucoma afflict patients around the world and rob them of their eyesight. Secondary glaucoma is induced by many factors, such as trauma to the eye, injury-induced inflammation, pathogen-induced inflammation, and drug-induced pathology of the major aqueous humor outflow system, the trabecular meshwork. When patients experience inflammation and irritation on the ocular surface or within the anterior chamber of the eye (e.g., uveitis), they are prescribed topical ocular formulation of corticosteroid (e.g., dexamethasone) and perhaps also oral antiinflammatory steroids to reduce the symptoms and calm down the eye. However, a major side effect of such corticosteroid treatment is the development of secondary glaucoma in at least 30% of the population who are susceptible to steroids. In order to find suitable remedies for this condition, a variety of animal models of steroid-induced ocular hypertension (OHT) have been developed for testing drugs and other therapeutics. Some of these models and techniques will be described in this chapter.
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