Atorvastatin improves hyperlipidemia-induced erectile dysfunction via PKA-associated eNOS phosphorylation at the Ser633 site

Introduction

Hyperlipidemia contributes to vasculogenic erectile dysfunction (ED) by reducing endothelial nitric oxide bioavailability. Although atorvastatin has been reported to improve ED, the upstream mechanism by which it restores endothelial nitric oxide synthase (eNOS) activity remains unclear. This study aimed to evaluate the therapeutic effect of atorvastatin in hyperlipidemia-induced erectile dysfunction (HLED) and to determine whether protein kinase A (PKA)-associated phosphorylation of eNOS at Ser633 contributes to this effect.