Introduction: Erectile dysfunction (ED) after radical prostatectomy (RP) is a very common condition. Prostacyclin (PGI(2)) is a prostaglandin with properties of vasodilation and anti-platelet aggregation. SuperEnzyme is a newly engineered protein with PGI(2) synthase activity that converts arachidonic acid directly to PGI(2). Transfection of SuperEnzyme into the penis to generate high levels of PGI(2) may increase penile blood inflow, alleviate hypoxia, and prevent apoptosis and fibrosis with potential use for ED after RP.
Aim: The pathophysiology of ED after RP and the prostaglandin regulation was reviewed, and the possibly relevant mechanism of SuperEnzyme as a therapy for ED after RP was proposed.
Main outcome measure: The rationale for SuperEnzyme as a possible therapy for ED after RP is analyzed.
Methods: We reviewed the publications on the proposed pathophysiology of ED after RP, the molecular regulation of prostaglandin and methods of SuperEnzyme engineering and transfection.
Results: ED after RP is involved in hypoxia, apoptosis and fibrosis, mainly due to the cavernosal nerve injury. Transfection of SuperEnzyme into the penis of an animal model to produce PGI(2) is feasible. Animal studies with the use of SuperEnzyme gene therapy are needed to provide new insight into metabolic and signaling pathways of PGI(2) in the penis and the role of PGI(2) signaling in the recovery of erectile function after RP.
Conclusion: SuperEnzyme may be a potential candidate as a gene therapy for ED after RP.