<p>Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) is characterized by chronic pelvic pain and urinary symptoms that imposes a significant quality-of-life burden, but the pathogenesis of this syndrome is poorly known, preventing effective therapy. Exosomes, small extracellular vesicles, which mediate cellular communication through proteins, cytokines, and miRNAs, are potent immune modulators that promote prostate inflammation and fibrosis. Simultaneously, dysregulated autophagy, a conserved degradation pathway essential for cellular homeostasis, is involved in the chronic inflammation and immune dysfunction characteristic of CP/CPPS. Critically, emerging evidence points to a bidirectional, functional crosstalk between exosome secretion and autophagic flux. This review proposes and critically evaluates the hypothesis that this ‘exosome-autophagy axis’ is a self-perpetuating process that contributes to immune dysregulation, neuroinflammation and tissue remodelling in CP/CPPS. We synthesize the limited direct data of the CP/CPPS with information extrapolated based on related conditions, establish particular cellular discussions that may operationalize this axis, and discuss its potential implications for future biomarker and therapeutic strategies.</p> Graphical Abstract <p></p>

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The exosome-autophagy axis: emerging mechanisms and therapeutic implications in type III prostatitis

  • Daniel Kofi Nyame,
  • Xiaohui Zhou

摘要

Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) is characterized by chronic pelvic pain and urinary symptoms that imposes a significant quality-of-life burden, but the pathogenesis of this syndrome is poorly known, preventing effective therapy. Exosomes, small extracellular vesicles, which mediate cellular communication through proteins, cytokines, and miRNAs, are potent immune modulators that promote prostate inflammation and fibrosis. Simultaneously, dysregulated autophagy, a conserved degradation pathway essential for cellular homeostasis, is involved in the chronic inflammation and immune dysfunction characteristic of CP/CPPS. Critically, emerging evidence points to a bidirectional, functional crosstalk between exosome secretion and autophagic flux. This review proposes and critically evaluates the hypothesis that this ‘exosome-autophagy axis’ is a self-perpetuating process that contributes to immune dysregulation, neuroinflammation and tissue remodelling in CP/CPPS. We synthesize the limited direct data of the CP/CPPS with information extrapolated based on related conditions, establish particular cellular discussions that may operationalize this axis, and discuss its potential implications for future biomarker and therapeutic strategies.

Graphical Abstract