# Current research hotspots and difficulties of chronic prostatitis/chronic pelvic pain syndrome: neuroendocrine mechanism

**Authors:** Bo Shao, Kaixiu Wu, Zhengkai Fan, Xingwu Gao, Shui Wan, Li Xiao, Yanggen Zuo, Jinbo Pi, Pingping Sun

PMC · DOI: 10.1080/07853890.2026.2616886 · Annals of Medicine · 2026-01-19

## TL;DR

This paper reviews recent research on how neuroendocrine mechanisms contribute to chronic prostatitis/chronic pelvic pain syndrome and suggests new treatment approaches.

## Contribution

The paper highlights novel neuroendocrine pathways and proposes precision medicine strategies for CP/CPPS.

## Key findings

- Neuroendocrine mechanisms like neuropeptides and HPA axis dysregulation play key roles in CP/CPPS.
- Gut–prostate axis interactions reveal new insights into neuroendocrine-immune communication.
- Targeting neuroendocrine pathways offers promising therapeutic directions for precision medicine.

## Abstract

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.

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.

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.

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.

## Full-text entities

- **Genes:** TAC1 (tachykinin precursor 1) [NCBI Gene 6863] {aka Hs.2563, NK2, NKNA, NPK, TAC2}
- **Diseases:** CP (MESH:D002972), inflammation (MESH:D007249), Chronic prostatitis (MESH:D011472), infection (MESH:D007239), neurogenic inflammation (MESH:D020078)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12821347/full.md

## References

45 references — full list in the complete paper: https://tomesphere.com/paper/PMC12821347/full.md

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Source: https://tomesphere.com/paper/PMC12821347