Abstract

Metabolic and endocrine disorders share a set of conserved pathogenic circuits in which oxidative stress and immune 
dysregulation are tightly intertwined. Benign prostatic hyperplasia (BPH), diabetes mellitus, and reproductive 
hormone imbalance provide complementary windows into this biology. Across these conditions, mitochondrial 
dysfunction, NADPH oxidase activity, advanced glycation end-products, and endoplasmic reticulum stress amplify 
reactive oxygen and nitrogen species, while innate and adaptive immune programs-Toll-like receptors, NLRP3 
inflammasome, macrophage polarization, and T-cell skewing-sustain chronic inflammation and fibrotic remodeling. 
Hormonal milieus modulate these redox–immune loops: androgens and estrogens shape stromal–epithelial crosstalk 
in the prostate; insulin and adipokines orchestrate hepato–renal injury in diabetes; and hypoestrogenism, 
hyperandrogenism, or hypogonadism recalibrate neuroimmune tone and metabolic flux. This review synthesizes 
mechanistic commonalities and disease-specific features, highlights organ and axis crosstalk (gut–liver–kidney
prostate–brain), and outlines a therapeutic framework combining metabolic control, redox restoration, and 
immunomodulation. We discuss biomarkers for stratification and monitoring and propose trial designs that test 
multi-target strategies across indications where shared biology predicts shared benefit. 
Keywords: oxidative stress, immunomodulation, benign prostatic hyperplasia, diabetes, reproductive hormones