Vascular aging-driven erectile dysfunction: pathophysiological mechanisms and emerging therapies-a narrative review

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)

Background and objective Age-related erectile dysfunction (ED) is a significant health concern linked to vascular aging, characterized by endothelial dysfunction and vascular smooth muscle alterations. This study aimed to explores the pathophysiological mechanisms of age-related ED in elderly men, providing new directions for diagnosis and the development of novel targeted therapies. Methods This review focused on literature from 2000 to 2025 concerning vascular aging and ED. We searched PubMed, Web of Science, and Embase using keywords like "erectile dysfunction", "aging", "vascular endothelium", and "vascular smooth muscle". The selection process prioritized high-quality clinical and innovative preclinical studies in humans or animal models that explored pathophysiology or novel treatments. Exclusion criteria included duplicates, non-peer-reviewed articles, and off-topic studies. Key content and findings Key contributors to age-related ED include reduced nitric oxide (NO) bioavailability due to endothelial oxidative stress and inflammation, diminished cavernosal smooth muscle content leading to impaired veno-occlusion, and increased arterial stiffness compounded by metabolic disorders. Chronic inflammation, oxidative stress, hormonal imbalances (particularly testosterone deficiency), and metabolic disruption accelerate these vascular aging processes, making ED an early indica

Evidence level

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

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