New Pathogenic Concepts and Therapeutic Approaches to Oxidative Stress in Chronic Kidney Disease

Figure 3

The pathophysiological mechanism of diabetic nephropathy and targets for emerging therapies. Advanced glycation end products (AGEs), endothelin-1 (ET-1), receptor for AGEs (RAGES), superoxide dismutase (SOD), catalase (CAT), nicotinamide adenine dinucleotide phosphate oxidase (NADPHox), glutathione (GSH), glutathione peroxidase (GPX), glutathione reductase (GR) and glutathione-s-transferase (GST), transforming growth factor-1 (TGF-1), tumor necrosis factor-α (TNF-α), reactive oxygen species (ROS), sodium-glucose cotransporter 2 (SGLT2), nuclear transcription factor-kappa-B (NF-B), vascular endothelial growth factor (VEGF), Monocyte Chemoattractant Protein (MCP-1), connective tissue growth factor (CTGF), fibronectin (FN), vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), heme oxygenase-1 (HO-1), NF-E2-related factor-2 (Nrf2), and collagen type IV (col IV).