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Updated: Apr 17, 2026

An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
Published on: April 7, 2014
Corneal neovascularization and contemporary antiangiogenic therapeutics
Chih-Chien Hsu1, Hua-Ming Chang2, Tai-Chi Lin1
1Department of Ophthalmology, Taipei Veterans General Hospital, Taipei, Taiwan, ROC; Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan, ROC.
Abstract:
Corneal neovascularization (NV), the excessive ingrowth of blood vessels from conjunctiva into the cornea, is a common sequela of disease insult that can lead to visual impairment. Clinically, topical steroid, argon laser photocoagulation, and subconjunctival injection of bevacizumab have been used to treat corneal NV. Sometimes, the therapies are ineffective, especially when the vessels are large. Large vessels are difficult to occlude and easily recanalized. Scientists and physicians are now dedicated to overcoming this problem. In this article, we briefly introduce the pathogenesis of corneal NV, and then highlight the existing animal models used in corneal NV research-the alkali-induced model and the suture-induced model. Most of all, we review the potential therapeutic targets (i.e., vascular endothelial growth factor and platelet-derived growth factor) and their corresponding inhibitors, as well as the immunosuppressants that have been discovered in recent years by corneal NV studies.
Insights
Corneal neovascularization (NV) causes vision loss and current treatments are often ineffective for large vessels. Research explores new therapeutic targets and inhibitors to improve treatment outcomes for this condition.
Area of Science:
- Ophthalmology
- Vascular Biology
- Regenerative Medicine
Background:
- Corneal neovascularization (NV) involves blood vessel growth into the cornea, impairing vision.
- Current treatments like steroids, laser photocoagulation, and bevacizumab injections show limitations, particularly for large, recalcitrant vessels prone to recanalization.
Purpose of the Study:
- To review the pathogenesis of corneal NV.
- To highlight established animal models for corneal NV research.
- To survey recent therapeutic targets, inhibitors, and immunosuppressants for corneal NV.
Main Methods:
- Literature review of corneal neovascularization pathogenesis.
- Analysis of existing animal models: alkali-induced and suture-induced.
- Survey of therapeutic strategies including growth factor inhibitors and immunosuppressants.
Main Results:
- Corneal NV is a significant cause of visual impairment with challenging treatment scenarios.
- Alkali-induced and suture-induced models are key tools for studying corneal NV.
- Vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) are identified as crucial targets.
Conclusions:
- Effective treatment of corneal NV, especially large vessels, remains a clinical challenge.
- Animal models are essential for advancing research into corneal NV.
- Targeting VEGF, PDGF, and exploring novel immunosuppressants offer promising avenues for future therapies.
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