الفهرس 
Aim of the WorkOnly 14 pages are availabe for public view
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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.