Critically, Prdx3 intersects with OS, pyroptosis, and autophagy pathways in BPH: (1) Prdx3 suppresses autophagy by reducing mitochondrial ROS, thereby preventing autophagic clearance of damaged organelles; (2) Autophagy deficiency activates NLRP3 inflammasomes and caspase-1, inducing pyroptosis; (3) Pyroptotic cell death releases inflammatory cytokines (e.g., IL-1β, IL-18) that stimulate compensatory prostate cell proliferation. Here, IL18 is linked to benign prostatic hyperplasia.