Research Advances in Stem Cell Therapy for Erectile Dysfunction

Abstract

Erectile dysfunction (ED) is a common clinical condition that mainly affects men aged over 40 years. Various causes contribute to the progression of ED, including pelvic nerve injury, diabetes, metabolic syndrome, age, Peyronie's disease, smoking, and psychological disorders. Current treatments for ED are limited to symptom relief and do not address the root cause. Stem cells, with their powerful ability to proliferate and differentiate, are a promising approach for the treatment of male ED and are gradually gaining widespread attention. Current uses for treating ED have been studied primarily in experimental animals, with most studies observing improvements in erectile quality as well as improvements in erectile tissue. However, research on stem cell therapy for human ED is still limited. This article summarizes the recent literature on basic stem cell research on ED, including cavernous nerve injury, aging, diabetes, and sclerosing penile disease, and describes mechanisms of action and therapeutic effects of various stem cell therapies in experimental animals. Stem cells are also believed to interact with host tissue in a paracrine manner, and improved function can be supported through both implantation and paracrine factors. To date, stem cells have shown some preliminary promising results in animal and human models of ED.

Fig. 1

Stem cells injected into the corpus cavernosum may act in three ways: 1. Stem cells migrate directly to the site of injury and differentiate into neuronal cells, endothelial cells, and smooth muscle cells; 2. stem cells may produce paracrine angiogenic factors, neurostimulatory factors, immunomodulatory factors, and anti-apoptotic factors; 3. stem cells may play a role in cytotoxicity by releasing microvesicles and exosomes.

Fig. 2

The microscopic mechanism of penis erection. GC guanylate cyclase, PKG protein kinase G, MLC myosin light chain, AC adenylate cyclase, PGE1 prostagtandin E1, NANC nonadrenergic noncholinergic, GTP guanosine triphosphate, cGMP cyclic guanosine monophosphate, NO nitric oxide, ATP adenosine triphosphate, AMP adenosine monophosphate, Ach acetylcholine, eNOS endothelial nitric oxide synthase, AKT protein kinase B, PDE5i phosphodiesterase 5 inhibitors, PDE5 phosphodiesterase 5, MLCP myosin light chain phosphatase