Mediators of Neovascularization and the Hypoxic Cornea

Abstract

The maintenance of corneal avascularity is essential to vision. The mechanisms by which the cornea becomes vascularized in response to inflammation or hypoxic stress are beginning to be elucidated. A detailed understanding of the molecular responses of the cornea to hypoxia is critical for prevention and development of novel treatments for neovascularization in a range of disease states. Here, we have examined the current literature on the major mediators of angiogenesis, which have previously been reported during hypoxia in the cornea in order to better understand the mechanisms by which corneal angiogenesis occurs in circumstances where the available oxygen is reduced. The normal cornea produces angiogenic factors that are regulated by the production of anti-angiogenic molecules. The various cell types of the cornea respond differentially to inflammatory and hypoxic stimuli. An understanding of the factors that may predispose patients to development of corneal blood vessels may provide an opportunity to develop novel prophylactic strategies. The difficulties with extrapolating data from other cell types and animal models to the cornea are also examined.

Keywords:

• angiogenesis
• arachidonic acid metabolites
• contact lenses
• cornea
• cytokines
• hypoxia