The Intersection of Benign Prostatic Hyperplasia and Reproductive Hormones: Oxidative Stress, Inflammation, and Immunomodulatory Pathway

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. Keywords: Benign prostatic hyperplasia, reproductive hormones, oxidative stress, inflammation, immunomodulation