Molecular mechanisms involved in varicocele-associated infertility

Abstract

Varicocele is a pathologic enlargement of the pampiniform venous plexus within the spermatic cord, a condition that is a common cause of impaired sperm production and decreased quality of sperm. While varicocele is the most common surgically correctable risk factor for male infertility, not all males with varicocele experience infertility. In fact, most men with varicocele have normal spermatogenesis. Despite its prevalence, the molecular mechanisms of varicocele and its effect on testicular function are yet to be completely understood. We postulate that men with varicocele-associated infertility could have preexisting genetic lesions or defects in molecular mechanisms that make them more susceptible to varicocele-mediated testicular injury affecting spermatogenesis.

Fig. 1

Summary of the molecular and genetic mechanisms identified to date that could contribute to the pathogenesis of varicocele-associated infertility. HIF-1α hypoxia-inducible factor-1α, PI3K phosphatidylinositol 3-kinase, HSPA2/5 heat shock protein A2/5, ATP5D adenosine triphosphate synthase (ATPase), delta subunit, L-VDCC α1 L-type voltage dependent calcium channel, α1 isotype, AR androgen receptor, SOD1 superoxide dismutase 1, GST-M1/T1 glutathione S-transferase M1/T1