Abstract
Erectile dysfunction (ED) is an important cause of reduced quality of life for men and their partners. Recent studies have found that cavernous nerve injury (CNI) during prostate cancer surgery and other pelvic surgery results in medically induced CNIED in more than 80% of patients. The efficacy of first- and second-line treatment options for ED is poor. A great deal of research has been devoted to exploring new methods of neuroprotection and nerve regeneration to save erectile function in patients with CNIED, especially in patients with cavernous nerve injury after prostate cancer surgery. In addition, such as neuromodulatory proteins, proimmune ligands, gene therapy, stem cell therapy, and the current cutting-edge low-energy shock wave therapy have shown advantages in basic research and limited clinical studies. In the context of today's modern medicine, these new therapeutic techniques are expected to be new tools in the treatment of cavernous nerve injury erectile dysfunction. This article presents the main causes, mechanisms, and treatment of cavernous nerve injury erectile dysfunction and combines them with new treatment strategies.
Highlights
Erectile dysfunction (ED) is a male sexual disorder in which there is repeated or persistent difficulty achieving or maintaining an erection with a prevalence of 30-64% in men aged 40 to 79 years
Erectile dysfunction has a variety of causes, and with the widespread introduction of pelvic surgery in recent years, a type of neurologically injurious erectile dysfunction is becoming a focus of urological research, namely, cavernous nerve injury erectile dysfunction (CNIED)
This study found no significant rebound in neuronal NO synthase (NOS) (nNOS)-positive nerve density after Phosphodiesterase type 5 inhibitors (PDE5i) treatment in CNIED patients [16]
Summary
Erectile dysfunction (ED) is a male sexual disorder in which there is repeated or persistent difficulty achieving or maintaining an erection with a prevalence of 30-64% in men aged 40 to 79 years. After CN injury, sphincter integrity is disrupted, nNOS-positive nerve density is reduced, continuity of the CN reflex pathway is reduced or lost, and NO expression, a signaling molecule that mediates relaxation of cavernous smooth muscle and maintains penile erection, is severely downregulated [15]. Phosphodiesterase type 5 inhibitors (PDE5i) have been the mainstay of treatment for CNIED for many years, and PDE5i has been used in various types of ED by increasing cGMP levels to counteract cavernous tissue fibrosis They have been shown to be effective in some populations, patients with CNIED are generally complex and PDE5i is extremely dependent on the NO pathway and only works in those with preserved nerves, resulting in poor efficacy [19].
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