Answers are grounded in this paper and cite their sources.
Chronic inflammation can remodel the prostatic tissue ecosystem and may increase susceptibility to prostate cancer (PCa); however, direct causal evidence linking chronic prostatitis (CP) to PCa is still lacking, and the mechanisms of sustained intercellular information transfer remain unclear. Exosomal miRNAs are stable, selectively packaged, and capable of multi-target regulation, enabling them to transmit inflammation-related signals among epithelial cells, immune cells, and stromal cells. Patients with CP, particularly chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), and those with PCa both exhibit aberrant exosomal miRNA profiles, and some of these miRNAs are associated with inflammatory responses, oxidative stress, immune regulation, epithelial–mesenchymal transition (EMT), and tumor microenvironment remodeling. This review summarizes current evidence on exosomal miRNAs in CP and PCa and proposes a testable working hypothesis: CP-associated exosomal miRNAs may act as molecular information carriers linking chronic inflammation and PCa by sustaining inflammation, reprogramming cellular states, and remodeling the local microenvironment, thereby promoting the formation of a tumor-prone tissue ecosystem. We also evaluate their potential as risk-stratification biomarkers and therapeutic targets, and highlight that long-term cohort studies, cell-of-origin tracing, and direct functional validation are critical to testing this hypothesis. Elucidating this mechanism may provide a theoretical basis for early identification and precision intervention of inflammation-associated PCa.
No takes yet. Share an insight, caveat, or question.
Shen et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: