Reactive oxygen species and endothelial function in diabetes

Abstract

An increasing body of evidence suggests that oxidant stress is involved in the pathogenesis of many cardiovascular diseases, including hypercholesterolemia, atherosclerosis, hypertension, heart failure and diabetes. Recent studies have also provided important new insights into potential mechanisms underlying the pathogenesis of vascular disease induced by diabetes. Glycosylation of proteins and lipids, which can interfere with their normal function, activation of protein kinase C with subsequent alteration in growth factor expression, promotion of inflammation through the induction of cytokine secretion and hyperglycemia-induced oxidative stress are some of these mechanisms. It is widely accepted that hyperglycemia-induced reactive oxygen species contribute to cell and tissue dysfunction in diabetes. A variety of enzymatic and non-enzymatic sources of reactive oxygen species exist in the blood vessels. These include NADPH oxidase, mitochondrial electron transport chain, xanthine oxidase and nitric oxide synthase. The present article reviews the effects of reactive oxygen species on endothelial function in diabetes and addresses possible therapeutic interventions.