Microvascular Endothelial Dysfunction in Patients with Obesity

Purpose of ReviewTo examine the state of the art on the pathogenesis of endothelial dysfunction in the microcirculation ofpatients with obesity, focusing on the complex relationship between the consolidated and the novel mechanisms involved in thisalteration.Recent FindingsHuman obesity is associated with vascular endothelial dysfunction, caused by a reduced nitric oxide availabilitysecondary to an enhanced oxidative stress production. Pro-inflammatory cytokine generation, secreted by perivascular adiposetissue, is a major mechanism whereby obesity is associated with a reduced vascular NO availability. Vasculature also represents asource of low-grade inflammation and oxidative stress which contribute to endothelial dysfunction in obese patients. Recently, adirect influence of arginase on endothelial function by reducing nitric oxide availability was demonstrated in small vessels frompatients with severe obesity. This effect is modulated by ageing and related to the high levels of vascular oxidative stress.SummaryOxidative stress, inflammation, and enzymatic pathways are important players in the pathophysiology of obesity-related vascular disease. The identification of new therapeutic approaches able to interfere with these mechanisms will result inmore effective prevention of the cardiovascular complications associated with obesity.