Penile fracture is a rare and underreported urological emergency, defined as traumatic rupture of the tunica albuginea of the corpus cavernosum. Most cases result from vigorous sexual intercourse or direct blunt trauma to an erect penis. While conservative management was once standard, high rates of long-term complications - including severe penile curvature, fibrotic plaques, and permanent erectile dysfunction (ED) - have led to a universal preference for immediate surgical repair. Although anatomical and physiological outcomes after surgery are well documented, the long-term psychosexual impact remains poorly characterised. Many patients report performance anxiety, fear of recurrence, and changes in sexual habits, but these experiences are often overlooked in favour of objective hemodynamic assessments. This scoping review aims to map and synthesise current evidence on functional, sexual, and psychosexual outcomes after surgical repair of penile fractures. Specifically, it examines the impact of surgical timing on erectile function, identifies independent risk factors for postoperative ED, and evaluates psychological effects on sexual satisfaction, relationship dynamics, and ejaculatory function. This review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews (PRISMA-ScR) framework. Comprehensive searches were conducted in PubMed/MEDLINE, EMBASE, the Cochrane Library, SCOPUS, and Web of Science. Data charting included patient demographics, injury mechanisms, diagnostic methods, surgical timing, and validated psychometric assessments across nine core studies. Immediate surgical intervention, ideally within 24 hours, is the gold standard and is associated with lower postoperative ED rates (6.5% to 16.5%) than delayed surgery (up to 42.9%) and conservative management (up to 52.9%). Independent predictors of poor outcomes include age over 50, urethral injury, bilateral corporal involvement, and tunical defects larger than 2 centimetres. Early repair reduces scarring and penile curvature. However, psychosexual outcomes remain complex. While erectile function is usually preserved, many patients experience psychogenic issues. Up to 77.5% report persistent fear of recurrence, and nearly 69% change their sexual habits. Changes in ejaculatory latency are also observed and correlate with higher depressive scores. Broad psychiatric screening tools do not show increased rates of clinical depression or generalised anxiety, indicating that psychological distress is specific to sexual performance and relationships. Immediate surgical repair remains the standard approach for preserving erectile function and anatomical integrity after penile fracture. However, postoperative recovery should not be assessed solely by structural or hemodynamic outcomes. The available evidence suggests that some patients experience persistent fear of recurrence, avoidance behaviours, performance anxiety, and reduced sexual confidence after repair. These findings highlight the need for more consistent assessment of psychosexual outcomes in follow-up studies. Multidisciplinary postoperative support, including psychological counselling, sexual health assessment, and partner-centred care, may be considered where clinically appropriate, but further research is needed to define optimal follow-up and rehabilitation strategies.

Benign prostatic hyperplasia (BPH) is increasingly linked to endothelial dysfunction, angiogenic activation, chronic inflammation, and metabolic dysregulation. This randomized controlled trial evaluated the dose-dependent effects of tadalafil on circulating endothelial, angiogenic, metabolic, and microRNA biomarkers implicated in BPH. A total of 306 sexually active men with BPH/LUTS and erectile dysfunction were randomized equally to placebo, tadalafil 2.5 mg, or tadalafil 5 mg daily for 12 weeks. Baseline demographic, clinical, biochemical, and molecular characteristics were comparable across groups. Tadalafil produced significant, dose-dependent improvements across multiple mechanistic domains. Both doses reduced circulating ANGPTL2, E-selectin, MMP-7, and PECAM-1, while increasing eNOS levels (p < 0.0001). Lipid metabolism improved, with favorable shifts in the Atherogenic Index of Plasma (AIP), decreasing from 0.65 in the placebo group to 0.62 with 2.5 mg and 0.50 with 5 mg tadalafil (p < 0.0001). Tadalafil also modulated microRNA expression, increasing hsa-miRNA-486-3p and decreasing hsa-miRNA-181a-5p in a dose-dependent manner (p < 0.0001). Clinical outcomes paralleled biomarker changes. Both tadalafil doses improved IPSS scores, with the greatest symptom relief at 5 mg. Biomarker-symptom correlations were strong, including ANGPTL2 (r = 0.6806-0.766), PECAM-1 (r = 0.892-0.896), eNOS (r = -0.655 to -0.824), hsa-miRNA-486-3p (r = -0.707 to -0.880), and HDL (r = -0.833 to -0.855). Tadalafil was well tolerated, with no treatment-related discontinuations. Tadalafil was associated with dose-dependent changes in endothelial, angiogenic, metabolic, and microRNA biomarkers. Because the study enrolled sexually active men with BPH/LUTS and erectile dysfunction, findings may not be generalizable to all men with BPH.

With global population aging, erectile dysfunction is becoming increasingly prevalent among middle-aged and older men, who frequently present with cardiometabolic comorbidities, such as hypertension and diabetes mellitus. Although these conditions are well-established risk factors for erectile dysfunction, their long-term pharmacological management may exert heterogeneous and adverse effects on erectile function, complicating clinical decision-making. This review synthesizes current evidence on the shared pathophysiological mechanisms linking erectile dysfunction with hypertension and diabetes mellitus, including endothelial dysfunction, oxidative stress, vascular remodeling, metabolic dysregulation, and neurovascular impairment. This review also critically evaluates the effects of commonly prescribed antihypertensive and antidiabetic drug classes on erectile function, highlighting both their beneficial and detrimental profiles. By integrating mechanistic insights with clinical evidence, this review highlights medication-associated sexual dysfunction in aging men. It emphasizes its recognition and management in clinical practice. The goal is to guide individualized treatment strategies that control cardiometabolic disease while preserving sexual health and quality of life.

Prostate, bladder, and corpus cavernosum share common pathophysiological mechanisms involving smooth muscle tone regulation through cyclic nucleotide signaling, particularly cAMP and cGMP pathways. Probenecid, a classical uricosuric agent, has emerged as a candidate for drug repurposing due to its ability to inhibit multidrug resistance-associated proteins 4/5 (MRP4/MRP5), which mediate the cellular efflux of cyclic nucleotides, as well as pannexin-1 channels, organic anion transporters, TRPV2 channels, and purinergic receptors. Given that lower urinary tract symptoms, benign prostatic hyperplasia, and erectile dysfunction frequently coexist and share overlapping signaling pathways, we hypothesized that probenecid could potentiate smooth muscle relaxation mediated by cAMP- or cGMP-elevating agents across these tissues. Using isolated rat bladder, prostate, and corpus cavernosum, we evaluated the functional effects of probenecid (0.1-1 mM) through concentration-response curves and intracellular cyclic nucleotide quantification. Probenecid potentiated relaxation induced by β-adrenoceptor agonists and adenosine in the bladder, accompanied by increased intracellular cAMP without changes in cGMP. In prostate, probenecid enhanced relaxation induced by cAMP- and cGMP-elevating agents and increased intracellular cAMP when combined with salbutamol. In corpus cavernosum, probenecid induced relaxation per se and potentiated responses to acetylcholine, sodium nitroprusside, phosphodiesterase inhibitors, and β-agonists, with concurrent increases in both cAMP and cGMP. Selective tools targeting OAT1/3, P2X7 receptor and TRPV2 channels did not replicate these effects, whereas pannexin-1 inhibition potentiated acetylcholine-induced relaxation only in the corpus cavernosum. In conclusion, probenecid modulates smooth muscle relaxation across urogenital tissues and may represent a potential adjunct in the treatment of lower urinary tract symptoms and erectile dysfunction.

Among poultry species, only waterfowl (e.g., goose and duck) possess the external genitalia. Normal erection of the external genitalia in male geese is directly related to mating capability, but its underlying genetic mechanisms remain elusive. In this study, we conducted a multi-omics study on male geese with normal erection (NE) and erectile dysfunction (ED) external genitalia phenotypic, to identify key candidate genes and main molecular networks contributing to external genitalia development differences. Here, we present a comprehensive genome resource for male geese, including a high-coverage (20×) whole genome of 259 samples from Sichuan White Goose × Lande Goose F2 resource population. The genome-wide association study (GWAS) analyses of NE and ED male geese indicated that PCDH7, TFPI, CALCRL, HIBCH, COL3A1, and CAVIN2 may be related to the differences in erectile function of external genitalia. At the transcriptomic level, we identified 318, 629, 2482, and 901 differentially expressed genes (DEGs) in the hypothalamus, pituitary gland, testis, and external genitalia cartilage between NE and ED groups, respectively. Further analysis demonstrated that PCDH7 was identified by both SNP-GWAS and transcriptomic analysis. Integrated with transcriptome data, it was revealed that PCDH7 involved in the function of male goose external genitalia cartilage development may be through MAPK signaling pathway. Collectively, our multi-faceted analysis suggests that PCDH7 affects male geese external genitalia erection may be through the MAPK signaling pathway. Our findings not only provide new insights into the development of external genitalia but also contribute to improving the reproductive performance of male geese.