Figure 5.

Mechanisms of ROS-induced endothelial dysfunction in response to hyperglycemia. Vascular damage caused by elevated glucose levels is mainly derived by an imbalance between ROS production and NO bioavailability in the endothelium and by the direct damaged caused by the accumulation of AGE. Resulting endothelial dysfunction is characterized by the activation of several deleterious mechanisms, including proinflammatory response, recruitment of leukocytes, accumulation of oxidized LDL particles and impaired vasodilatation, in the onset of cardiovascular complications. AGE: Advanced glycation end-products; eNOS: Endothelial nitric oxide synthase; LDL: Low density lipoprotein particles; NADPHox: Nicotinamide adenine dinucleotide phosphate oxidase; NO: Nitric oxide; O₂^•−: Superoxide anion; ONOO⁻: Peroxynitrite; PKC: Protein kinase C; RNS: Radical nitrogen species.