Publications

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–kidneyprostate–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