The normal cornea, the transparent "windscreen" of the eye, is devoid of both blood and lymphatic vessels. Nevertheless, both hem- and lymphangiogenesis can occur in response to severe corneal inflammation and can lead to blindness. Judah Folkman and co-workers exceedingly used the normally avascular cornea as the in vivo model system to study the mechanisms of angiogenesis and to test activators and inhibitors of angiogenesis in the last 3 decades. Recently, the cornea also became a successful model to study especially inflammatory lymphangiogenesis. As the last step in the circle from bedside to bench and back, we now are seeing the first (usually off-label) use of specific novel angiogenesis inhibitors in the diseased and pathologically vascularized human cornea to treat sight-threatening corneal angiogenesis and to promote graft survival after corneal transplantation by inhibiting lymphangiogenesis.
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Regenfuß et al. (2008) studied this question.
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