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Updated: Feb 28, 2026

An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
Published on: April 7, 2014
[Mechanisms of corneal neovascularization and modern options for its suppression]
V R Mamikonyan1, E A Pivin1, D A Krakhmaleva1
1Research Institute of Eye Diseases, 11 A, B, Rossolimo St., Moscow, Russian Federation, 119021.
Abstract:
Quite a number of pathological factors exist that can disturb the balance between anti-angiogenic and proangiogenic mechanisms, thus causing vascularization of the cornea. The neovessels are immature, ill-formed, and show increased permeability, which is dangerous of corneal edema, lipid deposition, and opacification. Moreover, as known, corneal neovascularization (CNV; preexisting or postoperative) may contribute to immune response against the transplant. Suppression of neovascularization is able to decrease the risk of corneal transplant rejection. In order to identify the principal strategy for struggling against CNV, we should first get a better understanding of its etiology, pathogenesis, and role in transplant immunity as well as mechanisms of action of available treatment methods.
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