Pathophysiology of Benign Prostatic Hyperplasia: Cellular and Molecular Mechanisms

Benign prostatic hyperplasia (BPH) is a prevalent condition among aging males, characterized by non-malignant enlargement of the prostate gland, which can lead to lower urinary tract symptoms (LUTS) and a significant reduction in quality of life. This review explores the cellular and molecular mechanisms underpinning the pathophysiology of BPH, highlighting the interplay of hormonal, inflammatory, and growth factor signaling pathways. Testosterone and dihydrotestosterone (DHT) serve as pivotal regulators of prostate growth, driving hyperplasia through androgen receptor-mediated transcriptional activity. Additionally, chronic inflammation, mediated by immune cell infiltration and cytokine release, contributes to tissue remodeling and stromal proliferation. Dysregulated growth factors such as fibroblast growth factors (FGFs) and transforming growth factor-beta (TGF-β) further amplify cellular proliferation and extracellular matrix deposition. Emerging evidence underscores the role of oxidative stress and mitochondrial dysfunction in exacerbating prostatic cellular senescence and genomic instability. This review also addresses the influence of stromal-epithelial interactions and the contribution of stem/progenitor cell niches in maintaining aberrant growth. Understanding these intricate mechanisms provides a foundation for identifying novel therapeutic targets aimed at mitigating BPH progression and associated symptoms. Keywords: Benign prostatic hyperplasia, cellular mechanisms, hormonal regulation, inflammation, growth factors, molecular pathways, therapeutic targets.