Abstract

Benign prostatic hyperplasia (BPH) is one of the most prevalent urological disorders in aging men, characterized by 
prostate gland enlargement, lower urinary tract symptoms, and impaired quality of life. While androgen-driven 
growth has traditionally been emphasized in its pathogenesis, emerging evidence highlights the intricate interplay 
between reproductive hormones, oxidative stress, inflammation, and immunomodulation. Hormonal imbalances 
involving androgens, estrogens, and gonadotropins regulate stromal-epithelial interactions, driving cellular 
proliferation and remodeling. Concurrently, oxidative stress induces lipid peroxidation, DNA damage, and cellular 
senescence within the prostate microenvironment. Chronic low-grade inflammation further amplifies disease 
progression, recruiting immune cells and perpetuating a cycle of cytokine release, growth factor activation, and 
fibrotic remodeling. Immunomodulatory pathways, including T-cell polarization and innate immune responses, have 
been increasingly implicated in the chronicity of BPH. This review synthesizes current evidence on the hormonal, 
oxidative, and immune-mediated drivers of BPH, discusses therapeutic implications, and highlights future directions 
for integrative interventions targeting both endocrine and immunological pathways.