Reversion of penile fibrosis: Current information and a new horizon

Abstract

Ageing has a detrimental effect on cavernous tissue and the tunica albuginea of the penis. Furthermore, atherosclerosis of the penile vessels that occurs with ageing causes a decrease in penile oxygen tension. A reduction in smooth muscle cells (SMCs) was shown in relation to diminution of oxygen tension. Chronic ischaemia is therefore not only associated with fibrosis but also with nitric oxide-cyclic guanosine monophosphate reduction. The sensitivity of the α-adrenoceptors on the SMCs increases with ageing. The decrease in penile elasticity and compliance are explained by the changes in the ratio of penile collagen that occur with ageing. Contradictory to the view that testosterone is only necessary for sexual desire, numerous recent studies showed that androgen deprivation produces penile tissue atrophy, alterations in dorsal nerve structure, alterations in endothelial morphology, reduction in trabecular SM content, increase in deposition of extracellular matrix and accumulation of fat-containing cells (adipocytes) in the subtunical region of corpus cavernosum. The aim of the current review is to shed some light on the underlying aetiology of corporal fibrosis especially ageing, cavernous nerve damage, androgen deprivation and tunical fibrosis. Ultimately I will address the proposed prevention of erectile dysfunction associated with penile fibrosis.

Keywords: (i)(e)NO(S), (inducible) (endothelial) nitric oxide (synthase); CVOD, corporal veno-occlusive dysfunction; Corpora cavernosa; ECM, extracellular matrix; ED, erectile dysfunction; Fibrosis; HIF-1α, hypoxia-inducible factor-1α; PD, Peyronie’s disease; PDE5-I, phosphodiesterase type 5 inhibitor; PGE, prostaglandin E; ROS, reactive oxygen species; SM(C), smooth muscle (cells); Tunica albuginea.