Publications

Benign prostatic hyperplasia (BPH) is a highly prevalent condition in aging men, historically attributed to androgenic stimulation and age-related tissue remodeling. Emerging evidence, however, suggests that metabolic dysfunction and systemic inflammation-particularly those associated with type 2 diabetes (T2DM), obesity, and metabolic syndrome-play influential roles in modifying prostate biology, driving stromal–epithelial proliferation, and promoting lower urinary tract symptoms (LUTS). This review synthesizes current knowledge on immune-metabolic dysregulation in BPH, focusing on how hyperglycemia, insulin resistance, chronic low-grade inflammation, oxidative stress, and adipokine imbalance modulate immune activation and prostate tissue remodeling. We examine mechanistic pathways linking diabetes to prostate enlargement, including altered insulin/IGF-1 signaling, inflammatory macrophage and T-cell infiltration, mitochondrial dysfunction, and redox imbalance. Particular attention is given to how metabolic disease reshapes immune phenotypes, such as promoting Th17 responses, senescence-associated secretory phenotypes (SASP), and pro-fibrotic myofibroblast activation, driving progression from benign hyperplasia to symptomatic obstruction. Finally, we discuss therapeutic implications, highlighting opportunities for metabolic therapies, anti-inflammatory interventions, antioxidant strategies, and microbiome-targeted approaches to modify disease trajectory. Understanding immune–metabolic crosstalk in BPH opens important avenues for precision medicine, especially in populations experiencing rising diabetes prevalence and associated inflammatory burden.