Regenerative technology for future therapy of erectile dysfunction

Ji-Kan Ryu, Jun-Kyu Suh


Although oral phosphodiesterase-5 (PDE5) inhibitors are generally an effective and well-tolerated therapy for erectile dysfunction (ED), such therapies are still far from curing ED and do not reverse the vasculopathic or neuropathic processes associated with ED. Moreover, certain populations with organic ED, such as that resulting from diabetes or radical prostatectomy (RP), respond poorly to PDE5 inhibitors. This reduced responsiveness to PDE5 inhibitors may be related to the severity of endothelial dysfunction or nerve damage. Because the effects of PDE5 inhibitors rely on endogenous nitric oxide (NO) formation, if the bioavailable NO is insufficient as the result of severe endothelial dysfunction or nerve damage, PDE5 inhibitors may fail to increase the level of cGMP above the necessary threshold.