18 Introduction Erectile dysfunction (ED) affects a large and growing proportion of adult men, with prevalence rising steeply from middle age. For four decades treatment has been dominated by on-demand pharmacology, chiey phosphodiesterase type 5 inhibitors (PDE5i), which are effective and safe but symptomatic: they potentiate an erection when taken, without altering the underlying vascular pathology. This leaves two persistent gaps. A meaningful minority of men respond poorly to or cannot tolerate oral therapy, and even successful users are managing a condition rather than modifying it. Low-intensity extracorporeal shockwave therapy (Li-ESWT) is the most clinically advanced of the interventions proposed to ll that gap. Adapted from the high-energy shockwave technology of urological lithotripsy but delivered at a fraction of the energy, it is intended to be restorative: to improve cavernosal blood ow by stimulating tissue regeneration rather than transiently relaxing smooth muscle. After more than a decade of randomised trials, the therapy sits in an unusual position. The mechanism is plausible, the measured effect is reproducible but modest, and guidelines cannot yet agree on how to classify it. This review summarises what the evidence shows, where it is strong, and where caution is required. Proposed mechanism of action The rationale for Li-ESWT is regenerative. Acoustic energy applied to the corpora cavernosa is thought to act through mechanotransduction, the conversion of mechanical shear stress into biological signalling, which triggers a cascade that promotes vascular repair. A systematic scoping review of 59 pre-clinical studies concluded that the therapy improves erectile function through several convergent pathways: stimulation of cellular mechanosensors, upregulation of angiogenic mediators such as vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS), neovascularisation and improved cavernosal microcirculation, recruitment of endothelial and mesenchymal progenitor cells, peripheral nerve regeneration, and reduction of local [1] inammation . The appeal is that, unlike a PDE5i, the intervention aims to remodel the vascular substrate of erection. The caveat is that the magnitude and consistency of these effects vary considerably with device type, energy ux density and treatment protocol, and no single denitive mechanism has been conrmed in humans. The biology supports clinical benet but does not prove it. Proposed mechanism of action of low-intensity focused shockwave therapy in erectile tissue STAGE 1 Focused acoustic shockwaves Applied to the corpora cavernosa STAGE 2 Mechanotransduction Shear stress on vascular endothelium activates cellular mechanosensors STAGE 3 Molecular signalling Up-regulation of VEGF, eNOS and other angiogenic mediators STAGE 4 Tissue regeneration Neovascularisation, progenitor cell recruitment, nerve regeneration, ↓ inammation OUTCOME Improved cavernosal blood ow & erectile function Figure 1. Proposed mechanism of action of low-intensity focused shockwave therapy in erectile tissue. Schematic representation. The strength and consistency of these effects vary with device type, energy ux density and protocol, so single mechanisms are likely oversimplied in humans. Original gure. Synthesised from Sokolakis et al., J Sex Med 2020.
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