# Research progress on the multidimensional mechanisms underlying impaired spermatogenesis induced by pathological microenvironment remodeling in chronic prostatitis

## TL;DR

This paper explores how chronic prostatitis disrupts sperm production through a complex network of inflammation, oxidative stress, and microbiome changes.

## Contribution

The study introduces a multidimensional framework linking inflammation, oxidation, endocrine, and microbiota pathways in impaired spermatogenesis.

## Key findings

- Chronic prostatitis causes inflammation and immune cell infiltration that hinder sperm development.
- Oxidative stress and ROS disrupt the antioxidant defense system in the spermatogenic environment.
- Microbiome alterations in the reproductive tract impair sperm function and maturation.

## Abstract

Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS), a prevalent urological and andrological condition among men of reproductive age, induces persistent pathological alterations. These alterations remodel the microenvironment of the prostate and reproductive tract through multiple pathways, thereby severely impairing sperm spermatogenesis, maturation, and function. By constructing a multidimensional interaction network encompassing “inflammation-oxidation-endocrine-microbiota, “ this article elucidates the four core pathological mechanisms by which the CP/CPPS microenvironment damages the full cycle of sperm development: (1) local inflammatory storms and immune cell infiltration hindering sperm development; (2) the collapse of the antioxidant defense system due to oxidative stress imbalance and excessive reactive oxygen species (ROS) generation; (3) metabolic homeostasis disruption in the spermatogenic microenvironment caused by neuroendocrine and biochemical disorders; and (4) sperm functional impairment resulting from heterogeneous alterations in the reproductive tract and gut microbiomes. This review systematically reveals the cascading impact of CP/CPPS on the entire chain of “testicular spermatogenesis–epididymal maturation–fertilization capacitation.” Furthermore, it posits that future research should focus on multi-omics mechanism resolution and shift towards a multi-target, precision combination intervention strategy of “anti-inflammation, antioxidation, endocrine regulation, and microecological reconstruction, “ providing a theoretical basis and translational direction for improving clinical reproductive outcomes in patients.