Metabolic syndrome (MetS) is an escalating epidemic that could influence
more than one billion people worldwide. It is expressed as the presence of visceral
obesity, hyperglycemia, dyslipidemia, and elevated blood pressure. MetS is a
multifactorial disorder affecting all features of the community and extensively affects
morbidity and mortality. Independently, the constituents of metabolic syndrome have
the potential to influence the endothelium causing vascular dysfunction and interrupt
vascular homeostasis. Since all components of MetS have unfavorable effects on the
endothelium, endothelial dysfunction is more prevalent in MetS patients. Endothelial
dysfunction could be a part of the pathogenesis of atherosclerosis in MetS. The
nominated mechanisms of endothelial dysfunction linked with MetS are reduced NO
production, upraised reactive oxygen species and high production of vasoconstrictors.
All the elements of MetS especially the compromised endothelial function could
participate in increasing the risks of cardiovascular disease, stroke, myocardial
infarction and type 2 DM. Endothelial dysfunction, moreover, stimulates proinflammatory and oxidative stress pathways via endothelial mitochondrial reactive
oxygen species (ROS) forcing vascular growth and remodeling. Because MetS is a
multifactorial disorder, numerous signaling pathways manipulate the succeeding
endothelial dysfunction. In the current review, we will discuss the incidence and
pathogenesis of altered endothelial function in MetS. We will also discuss the
impending effects of lifestyle measures and pharmacological interventions on
endothelial function in patients with MetS .
Keywords: Atherosclerosis, Endothelial dysfunction, Insulin resistance, Metabolic syndrome, Reactive oxygen species (ROS) .
