Abstract
Preeclampsia (PE) is a complex hypertensive disorder of pregnancy characterized by new-onset hypertension and proteinuria after 20 weeks of gestation. It is classified into early-onset (EOPE, <34 weeks) and late-onset (LOPE, ≥34 weeks) subtypes, which differ in their pathophysiology, clinical course, and maternal and neonatal outcomes. EOPE arises from abnormal placentation with inadequate spiral artery remodeling and impaired uteroplacental perfusion, whereas LOPE is mainly related to maternal cardiovascular and metabolic predisposition. This review integrates current molecular, immunological, and hemodynamic evidence distinguishing EOPE from LOPE, emphasizing recent insights into angiogenic imbalance (VEGF, PlGF, sFlt-1), oxidative stress, and immune modulation. It also summarizes evolving diagnostic and prognostic biomarkers and evaluates emerging therapeutic approaches, including gene therapy targeting placental dysfunction. By comparing mechanistic pathways and clinical implications, this review highlights how gestational age–specific pathogenesis may inform risk stratification, early detection, and precision-based management of PE.