Abstract

Benign prostatic hyperplasia (BPH) is a highly prevalent condition in aging men, historically attributed to 
androgenic and hormonal imbalances. However, mounting evidence supports a central role for the 
immune–prostate axis in its development. Chronic inflammation, immune-cell infiltration (e.g., T cells, 
macrophages), and sustained cytokine release contribute to a pro-proliferative microenvironment in the prostate. 
At the same time, oxidative stress (OS)-driven by excessive reactive oxygen species (ROS) from immune cells and 
metabolic dysregulation fosters tissue damage, DNA instability, and stromal-epithelial proliferation. The synergy 
of inflammation and OS disrupts apoptosis, enhances proliferation via MAPK, NF- κB, and STAT3 pathways, and 
triggers fibrotic remodeling. Emerging studies implicate deregulated antioxidant defense (e.g., diminished Nrf2 
activity), autophagy/ferroptosis imbalance, and immune-mediated signaling in the stromal expansion 
characteristic of BPH. This review synthesizes current mechanistic knowledge of the immune–prostate axis in 
BPH pathogenesis, highlights key molecular mediators, and discusses potential therapeutic strategies targeting 
inflammation and oxidative stress to complement conventional treatments.