The Concept of Preeclampsia in Biochemistry: Molecular Mechanisms, Oxidative Stress, and Emerging Biomarkers

Preeclampsia is a complex, pregnancy-related hypertension condition that significantly endangers mother and fetal health. While its clinical diagnosis is based on hypertension and proteinuria, its origins lie in a cascade of biochemical and molecular disturbances. This review highlights the central concept of preeclampsia from a biochemical perspective, with emphasis on abnormal placental development, oxidative stress, and endothelial dysfunction. Placental hypoxia and an excess of reactive oxygen species (ROS) are caused by inadequate spiral artery remodeling, which also leads to lipid peroxidation and systemic inflammation. A critical biochemical characteristic is the disparity between anti-antigenic (sFlt-1, sENG) and pro-antigenic (PlGF, VEGF) molecules, which leads to vascular damage and hypertension. The identification of novel biomarkers such as asymmetric dimethyl arginine, uric acid, and lipid peroxides holds promise for early diagnosis and targeted therapy. Understanding these biochemical pathways provides a foundation for developing personalized screening tools and improving therapeutic outcomes. This review integrates current advances in biochemical markers with clinical manifestations, aiming to refine preeclampsia early detection and management through a biomarker-driven approach.