Erectile dysfunction (ED) is a prevalent disorder in men and has a negative impact on quality of life. Recent studies have demonstrated that shear stress plays a critical role in modulating vascular endothelial function. Shear stress is categorized into physiological (e.g., laminar) and pathological (e.g., low shear or oscillatory) shear stress. This study reviewed current literatures on the relationship between share stress and ED, aiming to advance strategies for enhancing erectile function. Physiological shear stress increases the production of nitric oxide by activating endothelial nitric oxide synthase, thereby maintaining vascular homeostasis and erectile function. However, pathological shear stress exacerbates inflammation and oxidative stress, inducing endothelial dysfunction and ED. Shear stress also regulates gene expression, cell behavior, and signaling pathways in endothelial cells through multiple mechanisms, ultimately influencing erectile function. Studies indicate that exercise improves endothelial function and mitigates oxidative stress and inflammation by inducing shear stress, thereby offering novel therapeutic avenues for ED. Future research should focus on elucidating shear stress-mediating regulatory mechanisms, and developing diagnostic and therapeutic strategies to improve clinical outcomes in patients with ED.

Keywords: endothelial function; erectile dysfunction; inflammation; nitric oxide; shear stress