Oxidative Stress-Driven Prostatic Remodeling: Pathogenic Pathways and Therapeutic Targets

Ahereza Prissy

Department of Pharmacy Kampala International University Uganda

Email: prissy.ahereza@studwc.kiu.ac.ug

                                                                   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.

Keywords: oxidative stress, prostatic remodeling, benign prostatic hyperplasia, inflammation, redox signaling.

CITE AS: Serunjogi Ruth (2026). Oxidative Stress-Driven Prostatic Remodeling: Pathogenic Pathways and Therapeutic Targets. NEWPORT INTERNATIONAL JOURNAL OF SCIENTIFIC AND EXPERIMENTAL SCIENCES, 7(2):101-106. https://doi.org/10.59298/NIJSES/2026/72.101106