Vascular complications of diabetes represent the leading cause of morbidity and mortality in affected patients. Production of reactive oxygen species is increased in diabetic patients, especially in those with poor glycemic control. Reactive oxygen species affect vascular smooth muscle cell growth and migration, endothelial function, including abnormal endothelium-dependent relaxation and expression of a proinflammatory phenotype, and modification of the extracellular matrix. All of these events contribute to the development of diabetic microvascular and macrovascular complications, suggesting that the sources of reactive oxygen species and the signaling pathways that they modify may represent important therapeutic targets.