Redox biology in PCOS: Biomarkers, mechanistic networks, and targeted interventions (Review)

Polycystic ovary syndrome (PCOS) is a lifelong endocrine‑metabolic disorder affecting 11‑13% of women worldwide. Beyond ovulatory dysfunction, hyperandrogenism, and polycystic ovarian morphology, PCOS is tightly linked to insulin resistance, dyslipidemia, hypertension, and increased cardiometabolic risk. Converging evidence places oxidative stress at the core of PCOS pathophysiology, but current evidence should be interpreted in a phenotype‑aware manner. Obese, hyperandrogenic, and Rotterdam phenotype A/B presentations generally carry a heavier systemic oxidant‑inflammatory burden than phenotype D, whereas lean PCOS may still exhibit clinically relevant local ovarian redox abnormalities despite a milder metabolic background. Mitochondrial dysfunction, insulin resistance, and androgen excess amplify reactive oxygen species generation, while granulosa‑cell mitochondrial depolarization, apoptotic signaling, and NF‑κB‑driven inflammation degrade follicular fluid quality, oocyte competence, and embryo development. However, the literature remains heterogeneous because assay platform, specimen type, cycle phase, adiposity, and treatment exposure all influence biomarker reproducibility and comparability. In addition, most human research supports association, whereas stronger causal support comes from interventional or mechanistic research showing that modulation of NADPH oxidase 4, antioxidant pathways, mitochondrial function, or sex hormone‑binding globulin‑related oxidative signaling can alter key reproductive and metabolic phenotypes. To improve translational value, the present review prioritizes a core biomarker panel spanning serum/plasma and follicular fluid, distinguishes systemic oxidative markers from local ovarian microenvironmental markers, and critically compares antioxidant and metabolic interventions by evidence level, sample size, endpoint type, and major limitations. Recent phenotype‑oriented and multi‑omics reearch is further integrated to propose a biomarker‑guided framework for phenotype‑stratified trials and precision management of PCOS.