Abstract
Erectile dysfunction (ED) has been defined as the inability to attain or maintain penile erection sufficient for successful sexual intercourse. ED carries a notable influence on life quality, with significant implications for family and social relationships. Because atherosclerosis of penile arteries represents one of the most frequent ED causes, patients presenting with it should always be investigated for potential coexistent coronary or peripheral disease. Up to 75% of ED patients have a stenosis of the iliac-pudendal-penile arteries, supplying the male genital organ’s perfusion. Recently, pathophysiology and molecular basis of male erection have been elucidated, giving the ground to pharmacological and mechanical revascularization treatment of this condition. This review will focus on the normal anatomy and physiology of erection, the pathophysiology of ED, the relation between ED and cardiovascular diseases, and, lastly, on the molecular basis of erectile dysfunction.
Highlights
The release of norepinephrine from sympathetic neurons stimulates and maintains the flaccidity by releasing alpha-1 G-protein receptors on SMCs of the cavernous sinusoids, which activates calcium ions decrease in the intra-cytoplasmic reticulum and subsequent relaxation of smooth muscle cells themselves
PDE5i promote reverse remodeling and reduce myocardial apoptosis, fibrosis and hypertrophy [49,64,65]. Those cardiovascular beneficial effects were stronger in patients with prior myocardial infarction (MI) and were associated with reduced incidence of new MI, raising the possibility that PDE5is could prevent both complications post-MI and future cardiovascular events [66] (Figure 4) In particular, in a Swedish nationwide cohort study, 43.145 men
Erectile dysfunction is common in cardiovascular diseases (CVD) patients, and it is clear that it may represent a significative earlier predictor of cardiovascular events and cardiovascular death
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Has reported a prevalence of ED (complete and incomplete) of 12.8% and a significant incidence of age-related ED (2% between 18 and 30 years and 48% over 70 years) [5]. Data, over a population range between 40 and 70 years, ED increased with age from 5.1% to. The prevalence of ED worldwide will be estimated to reach 322 million men by 2025 [6]. This review will summarize the mechanism of men’s erection, focusing on pathophysiology and molecular mechanisms of erectile dysfunction, with a glimpse of the clinical linkage between cardiovascular disease and ED
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