Diabetes affects approximately 16 million people in the United States, of which 25% have diabetes-related microvascular complications, such as diabetic retinopathy. Diabetic retinopathy is a diabetic eye disease caused by damage to the small blood vessels of the retina in the back of the eye. The small vessels can be damaged by high blood glucose and high blood pressure, causing them to leak, which then leads to impaired vision. Diabetic retinopathy is a leading cause of blindness in adults. Currently available treatments, such as laser surgery and vitrectomy, are invasive and only palliative in nature.
Research has shown that increased levels of vascular endothelial growth factor (VEGF) and tumor necrosis factor (TNF) may contribute to the pathogenesis of diabetic retinopathy and increase leakage into the eye via activation of protein kinase C (PKC). Various compounds have been developed to potentially inhibit the deleterious action of factors such as VEGF and TNF, yet none have demonstrated highly significant efficacy in vivo, or the ability to prevent disease progression. Investigators at the University of Michigan have identified a novel class of atypical PKC inhibitors that prevent factor-induced leakage across the blood-retinal barrier. This technology was able to completely inhibit retinal endothelial cell permeability after VEGF treatment. In vivo studies reveal that these compounds can inhibit retinal breakdown after VEGF administration. Therapeutic application of novel atypical PKC inhibitors may prove to be a highly effective clinical treatment for microvascular diabetic complications.
- Treatment of diabetic retinopathy, with potential application to other microvascular complications
- High specificity (low dose required for effect)