The pathogenesis of diabetic nephropathy remains poorly defined, and animal models that
represent the human disease have been lacking. It was demonstrated recently that the
severe endothelial dysfunction that accompanies a diabetic state may cause an uncoupling
of the vascular endothelial growth factor (VEGF)-endothelial nitric oxide (eNO) axis, resulting
in increased levels of VEGF and excessive endothelial cell proliferation. It was hypothesized
further that VEGF-NO uncoupling could be a major contributory mechanism that leads to …