Metabolic Syndrome-Associated Erectile Dysfunction: Multiple Vascular Endothelial Dysfunction Mechanisms and Potential Therapeutic Targets

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Metabolic syndrome (MetS) causes vascular structural abnormalities, nerve damage, hormonal level changes and other lesions, which promote the occurrence and development of erectile dysfunction (ED). Penile vascular endothelial dysfunction is an important pathological feature of MetS-associated ED, and has received increasing attention in recent years. MetS negatively affects penile cavernous vascular function through the synergistic effects of insulin resistance, dyslipidemia, hypertension and obesity. The multiple pathological process may lead to impaired endothelium-dependent vasodilation, progressive fibrosis and reduced penile vascular blood flow reserve. This review summarized several common mechanisms of penile vascular endothelial dysfunction in MetS-associated ED, deeply discussed the roles of common pathological manifestations of MetS such as glucose metabolism disorder, hypertension, dyslipidemia and obesity on penile vascular endothelium, and explored treatments targeting these mechanisms in order to provide potential therapeutic targets and strategies in patients with MetS-associated ED.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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