Role of Inflammation and Oxidative Stress in Benign Prostatic Hyperplasia Progression

Benign prostatic hyperplasia (BPH) is a common urological condition affecting aging men, characterized by the non-malignant enlargement of the prostate gland, which often leads to lower urinary tract symptoms (LUTS). While hormonal changes and age are recognized as primary risk factors, the roles of chronic inflammation and oxidative stress in the progression of BPH have garnered significant attention. Chronic inflammation contributes to prostatic tissue remodeling and fibrosis, driven by inflammatory cytokines, immune cell infiltration, and pro-inflammatory signaling pathways. Oxidative stress, resulting from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, exacerbates cellular damage, amplifying inflammatory responses and promoting tissue dysfunction. This article explores the molecular mechanisms underlying inflammation and oxidative stress in BPH progression, highlights their interconnection, and discusses potential therapeutic strategies targeting these processes to mitigate disease progression and associated symptoms. Keywords: Benign prostatic hyperplasia (BPH), inflammation, oxidative stress, reactive oxygen species (ROS), cytokines, prostate enlargement