Annals of medicine · 2026
Current research hotspots and difficulties of chronic prostatitis/chronic pelvic pain syndrome: neuroendocrine mechanism.
СтатьяОбзорПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Shao Bo, Wu Kaixiu, Fan Zhengkai, Gao Xingwu, Wan Shui, Xiao Li, Zuo Yanggen, Pi Jinbo, Sun Pingping
Аннотация
BACKGROUND: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) presents a significant clinical challenge in urology. Traditional pathophysiological models emphasize infection and local inflammation; however, the limited efficacy of conventional therapies suggests the involvement of deeper regulatory mechanisms.
METHODS: This comprehensive review synthesizes evidence from the past five years regarding neuroendocrine pathways in CP/CPPS. We systematically analyzed literature from the PubMed, Web of Science, and CNKI databases, focusing on neuropeptide functions, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, sympathetic nervous system (SNS) signaling, glial cell activation, and gut-prostate axis interactions.
RESULTS: Neuroendocrine mechanisms significantly contribute to the pathophysiology of CP/CPPS through multiple pathways. Substance P and calcitonin gene-related peptide promote neurogenic inflammation, while B-type natriuretic peptide exhibits analgesic effects. Dysregulation of the HPA axis and sympathetic overactivation create stress-related imbalances. Central glial cell activation leads to central sensitization, and the emerging concept of the gut-prostate axis reveals bidirectional neuroendocrine-immune communication.
CONCLUSIONS: CP/CPPS is a systemic condition involving complex neuro-endocrine-immune interactions. Therapeutic strategies targeting neuroendocrine mechanisms-including neuropeptide receptor antagonists, glial cell inhibitors, and neuromodulation techniques-offer promising directions for precision medicine. Future research should focus on multi-omics approaches and neuroendocrine-based patient classification for individualized treatment.
METHODS: This comprehensive review synthesizes evidence from the past five years regarding neuroendocrine pathways in CP/CPPS. We systematically analyzed literature from the PubMed, Web of Science, and CNKI databases, focusing on neuropeptide functions, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, sympathetic nervous system (SNS) signaling, glial cell activation, and gut-prostate axis interactions.
RESULTS: Neuroendocrine mechanisms significantly contribute to the pathophysiology of CP/CPPS through multiple pathways. Substance P and calcitonin gene-related peptide promote neurogenic inflammation, while B-type natriuretic peptide exhibits analgesic effects. Dysregulation of the HPA axis and sympathetic overactivation create stress-related imbalances. Central glial cell activation leads to central sensitization, and the emerging concept of the gut-prostate axis reveals bidirectional neuroendocrine-immune communication.
CONCLUSIONS: CP/CPPS is a systemic condition involving complex neuro-endocrine-immune interactions. Therapeutic strategies targeting neuroendocrine mechanisms-including neuropeptide receptor antagonists, glial cell inhibitors, and neuromodulation techniques-offer promising directions for precision medicine. Future research should focus on multi-omics approaches and neuroendocrine-based patient classification for individualized treatment.