The pathogenesis of endothelial dysfunction

Endothelial dysfunction is the most common pathological feature of diabetes, hypertension and atherosclerosis. Endothelial dysfunction can occur not only in large conduit arteries such as aorta and renal artery, but also in microvascular circulation in the retina and kidney. Decreased production and secretion of endothelium-derived vasodilator factors (mainly nitric oxide) or increased synthesis and release of vasoconstrictor factors (such as angiotensin II, endothelin-1, reactive oxygen species and cyclooxygenase metabolites) are the main causes of endothelial dysfunction, which is closely associated with pathogenesis of hypertension, diabetes, atherosclerosis, myocardial ischemia, and heart failure. This review briefly summarizes the mechanisms underlying endothelial dysfunction in relation to activation of the renin angiotensin system, cyclooxygenase 2, and bone morphogenetic protein 4, as well as increased oxidative stress and inflammatory response in blood vessels, hoping to identify the key molecular mediators of endothelial dysfunction, thereby providing new clues for both basic and translational research in cardio-metabolic biology and medicine.