The isozyme protein kinase C (PKC) β is involved in several processes that are deregulated in different retinal cell types by hyperglycemia. This family of serine/threonine-specific protein kinases comprises several different members, which differ in their structure, cofactor requirement and substrate specificity. Therefore, PKCβ was considered a valuable target for therapeutic intervention. However, there is now evidence that even inhibition of different PKC isozymes is not sufficient to normalize vascular endothelial growth factor (VEGF)-induced barrier damage of retinal endothelial cells. On the other hand, PKCβ inhibition prevents hyperglycemia-induced VEGF expression in retinal pericytes, suggesting that PKC inhibitors should be administered before increased VEGF expression is established in the diabetic retina. Although initial studies have indicated that the treatment of diabetic patients with ruboxistaurin, a specific inhibitor of PKCβ, may reduce visual loss in patients with diabetic retinopathy, the overall benefit seems to be small.
© 2016 S. Karger AG, Basel.