Abstract

Corneal neovascularization (CNV) results from the growth of new vessels from the limbal vasculature into the normally avascular cornea. As the second cause of severe visual impairment worldwide, it represents a major clinical problem. This occurs because CNV often leads to corneal opacification, thus reducing visual acuity. CNV is a well characterized and complex process, which includes different aspects of the corneal tissue: degradation of the epithelial basement membrane, remodeling of the extracellular matrix (ECM), and proliferation of endothelial cells. A number of studies have investigated the molecular mechanisms regulating corneal angiogenesis, and various mechanisms have been identified. This paper will review corneal neovascularization and its relevance to human disorders. Additionally, we will describe experimental models commonly used to study CNV, the role of innate immune cells in inflammatory-induced angiogenesis, current therapies, and future directions.

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