الفهرس | Only 14 pages are availabe for public view |
Abstract Erectile dysfunction (ED) is characterized as the inability to achieve or maintain an erection to complete sexual intercourse or another chosen sexual activity sufficiently. It is known that ED is more widespread in patients with type 2 diabetes mellitus and metabolic syndrome. In a pathophysiological cascade responsible for endothelial dysfunction plays a role an impaired vascular nitric oxide (NO) synthesis and impaired vasodilatation through increased inflammation and oxidative stress. Erectile dysfunction (ED) and cardiovascular diseases have the same risk factors as hypertension, diabetes mellitus, hypercholesterolemia and smoking. The severity of erectile dysfunction correlates with the cardiovascular risk of patients and represents the early symptom of generalized atherosclerosis. ED can also be considered as a marker of early subclinical coronary artery damage and thus as an independent predictor of future cardiovascular events. NO bioavailability may be decreased by suppressed endothelial nitric oxide synthase (eNOS) expression and/or activity or by increased NO scavenging, for example, by superoxide formed during increased oxidative stress. Oxidative stress is a key pathogenic factor in the development of diabetic complications. During chronic hyperglycemia, advanced glycation end products (AGEs) are formed. AGEs bind covalently to the vascular collagen leading to thickening of the vascular wall, decreased elasticity, endothelial dysfunction and atherosclerosis. ROS are involved in many mechanisms of initiation or maintenance of functional and structural damage to cells and the entire organism. Increased oxidative stress and expression of inflammatory markers are seen in patients with diabetic ED. Endoglin, which is a 180 kDa homodimeric integral membrane glycoprotein, is involved in the regulation of endothelial function, serving as a receptor for the transforming growth factor-beta superfamily involved in the atherosclerotic processes. A soluble form of endoglin (S-endoglin), formed by the cleavage of the extracellular domain of the entire endoglin molecule, has been also suggested as a marker of endothelial dysfunction. S-endoglin was found to be increased in the serum of patients with type 2 DM and positively correlated with the severity of diabetic vascular changes. |