Corneal neovasculariation: a translational perspective

Development of corneal neovascularization (CNV) is a common finding in a number of disorders affecting the ocular surface. The role of infiltrating inflammatory cells, and specifically macrophages, is well described and associated with the development of CNV. Although CNV is commonly regarded as an ominous clinical sign due to its common association with vision reduction, the growth of neovessels can also beneficial in some instances. For example, CNV helps recruiting cellular immunity and provides protection against ocular perforation in corneal infections. Hence, avascularity of the cornea, constantly exposed to the outer environment, is the result of an evolutionary compromise between a prompt and effective reaction to aggression from the outside and the avoidance of corneal opacification. Specifically, the absence of vessels in the normal cornea is generally considered the result of the predominance of anti-angiogenic over pro-angiogenic factors. In this paper, we suggest a novel mechanism regulating corneal avascularity and its switch to corneal neovascularization. Potential translational implications are also discussed.