A novel approach to bladder dysfunction induced by bladder outlet obstruction: Low-intensity extracorporeal shock wave therapy promotes bladder regeneration.

Bladder outlet obstruction (BOO) leads to bladder structural and functional changes, including elevated detrusor contractile pressure, detrusor hypertrophy, fibrosis, and impaired contractility. Currently, no effective therapeutic strategy for BOO-induced bladder dysfunction. This study investigated whether low-intensity extracorporeal shock wave therapy (LiESWT) could improve bladder function by promoting detrusor contractility, urothelial proliferation, angiogenesis, and neurogenesis in a rat model of partial BOO (PBOO). Male Sprague-Dawley rats were divided into sham and PBOO groups for 4 or 8 weeks, with or without LiESWT once or twice weekly for 4 weeks. Urodynamic function, bladder histology, and the molecular mechanism were assessed. Compared to sham group, PBOO rats displayed wall hypertrophy, overdistension, mucosal damage, interstitial fibrosis, and altered microvascular patterns. However, LiESWT improved bladder structure, contractility, urothelial proliferation, tight junction restoration, mucosal regeneration, angiogenesis, and neurogenesis, while modulating muscarinic and purinergic receptors, transient receptor potential vanilloid (TRPV) channels, and signaling proteins (Gq/11, Gq/12, Gq/13, RhoA, RhoK, Erk1/2, p-Erk1/2, P38, p-P38, Akt and p-Akt). In conclusion, PBOO induced significant bladder dysfunction, marked by increased micturition frequency, reduced volume, and impaired contractility, whereas the effect was limited in the decompensated stage. However, LiESWT improved bladder compliance and contractile function in PBOO-related dysfunction at the hypertrophy/compensation stage.