Abstract

Oxidative stress has emerged as a central pathogenic mechanism in prostatic remodeling, particularly in benign 
prostatic hyperplasia (BPH) and other age-associated prostate disorders. Characterized by an imbalance between 
reactive oxygen species generation and antioxidant defense capacity, oxidative stress contributes to chronic 
inflammation, cellular senescence, extracellular matrix remodeling, and dysregulated epithelial–stromal 
interactions within the prostate. Accumulating experimental and clinical evidence indicates that sustained redox 
imbalance promotes prostatic enlargement through activation of redox-sensitive signaling pathways, including 
nuclear factor kappa B, mitogen-activated protein kinases, and transforming growth factor beta signaling. These 
pathways drive fibroblast-to-myofibroblast differentiation, smooth muscle hypercontractility, and excessive matrix 
deposition, collectively leading to structural and functional alterations of prostatic tissue. Moreover, oxidative 
stress intersects with metabolic dysfunction, hormonal imbalance, and immune dysregulation, amplifying disease 
progression and symptom severity. This review synthesizes current knowledge on the sources of oxidative stress 
in the prostate, delineates the molecular mechanisms linking redox imbalance to tissue remodeling, and evaluates 
emerging therapeutic strategies targeting oxidative and inflammatory pathways. Understanding oxidative 
stress–driven prostatic remodeling offers opportunities for novel interventions aimed at slowing disease 
progression and improving clinical outcomes.