Retinopathies develop in at least 50% of all diabetics, and the incidence increases with the duration of disease. More than 90% of individuals who have suffered diabetes for greater than 20 years have some degree of retinopathy. This aspect of diabetes has become the leading cause of blindness in the United States in middle-aged adults and overall is second only to retinal degeneration of the aged in terms of causes of visual loss. The economic costs can be massive, amounting to over $10,000 per year per person if blindness occurs. Screening and laser treatment are front-line approaches to retinopathy and have reduced the incidence of blindness and associated costs significantly however pharmaceutical options continue to be sought. Retinopathies occur as non-proliferative disease following blood vessel leakage, while proliferative retinopathy occurs as a result of abnormal angiogenesis. Vascular endothelial growth factor (VEGF) is accepted as a target for both types of retinopathy however due to the physiological and pathophysiological role of this growth factor, VEGF antagonists can evoke unwanted side effects. Since VEGF can bind to a number of different subtypes, the identification of specific subtypes involved in the pathological process could increase the therapeutic margin of drug candidates. Thus Dutch researchers have profiled the expression of VEGF receptors in human diabetic retinas. In control human retinas, all three VEGFRs were expressed in nonvascular areas, but only VEGFR-1 was constitutively expressed in retinal microvessels, suggesting physiological functions of VEGFs that do not involve the vasculature. In diabetic eyes, increased microvascular VEGFR-2 expression was found in leaky microvessels, whereas microvascular VEGFR-3 was present in a subset of leaky microvessels, suggesting that either (or both) of these receptors may offer an appropriate target for diabetic retinopathy.

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