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Updated: Jun 17, 2026

An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
Published on: April 7, 2014
[Mechanisms and regulation of corneal neovascularization]
1Department of Ophthalmology, University of Tokyo, Japan. tomohiko-tky@umin.ac.jp
Abstract:
The cornea is a transparent tissue and its transparency is dependent on many factors including avascularity. However, in response to a stimulation such as inflammation, neovasculature from the limbal plexus can invade the transparent cornea. Neovascularization in the corneal tissue induces unwanted opacification, which can result in significant reduction in visual function. Furthermore, corneal neovascularization is the main risk factor for rejection after keratoplasty. Although anti-angiogenic therapy is a promising approach to reduce corneal opacity and immune rejection secondary to keratoplasty, the exact mechanism driving corneal neovasuclarization has not been fully identified. In this review, we summarize the known mechanisms of corneal neovascularization and describe the involvement of macrophage migration inhibitory factor and the tissue rennin angiotensin system. Regulation of these factors can have immense therapeutic potential for the treatment and prevention of corneal neovascularization.
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