Diabetic retinopathy is a leading cause of blindness in the United States. Most severe visual loss associated with diabetes is related to the development of neovascularization of retinal vessels, with the potential for vitreous hemorrhage, retinal detachment, and other complications. It is thought that hypoxia serves as a stimulus for angiogenesis, but until recently the mechanism by which hypoxia-related neovascularization occurs has been unclear. In the past 2 years evidence has accrued that vascular endothelial growth factor (VEGF) may be a major component in this process.
Specifically, samples of ocular fluids from eyes of patients with proliferative diabetic retinopathy and other proliferative disorders contain elevated levels of VEGF, sufficient to cause neovascularization.1,2 In monkeys, development of iris neovascularization induced by laser retinal vein occlusion parallels a rise in aqueous humor and retinal VEGF,3 and neutralizing antibodies to VEGF block this rise.4 The time course is rapid; messenger
Levin LA. Ophthalmology. JAMA. 1996;275(23):1834-1836. doi:10.1001/jama.1996.03530470062037