[Retracted] PKCδ Promotes High Glucose Induced Renal Tubular Oxidative Damage via Regulating Activation and Translocation of p66Shc

Figure 8

Schematic drawing depicting PKCδ mediates p66Shc phosphorylation and mitochondrial translocation induced by HG. With treatment of HG, PKCδ is activated, promoting p66Shc phosphorylation and its translocation to mitochondria, where p66Shc oxidizes mCyt.C to induce mitochondrial ROS generation, which results in oxidative damage and apoptosis of renal tubular epithelial cells.