PATHOGENESIS OF PLACENTAL DYSFUNCTION IN PREECLAMPSIA AND FETAL GROWTH RESTRICTION: THE ROLE OF ENDOTHELIAL DYSFUNCTION AND VASCULAR MECHANISMS

Abstract

Placental dysfunction is a central pathogenetic mechanism underlying preeclampsia and fetal growth restriction (FGR), which remain leading causes of maternal and perinatal morbidity and mortality worldwide. These conditions are primarily associated with impaired trophoblast invasion and inadequate remodeling of spiral arteries, resulting in high-resistance uteroplacental blood flow. Endothelial dysfunction plays a pivotal role in this process and is characterized by angiogenic imbalance, activation of the coagulation cascade, and systemic inflammatory response.

The aim of this study is to analyze current concepts of vascular and molecular mechanisms of placental dysfunction, with a particular focus on endothelial function and angiogenic factors. Changes in levels of sFlt-1, PlGF, and VEGF and their impact on vascular tone and placental perfusion are discussed. Special attention is given to the role of hemostasis and immune factors, including regulatory T cells.

The findings demonstrate that integration of laboratory biomarkers, ultrasound data, and clinical parameters significantly improves early diagnosis and prediction of pregnancy complications. These results highlight the importance of developing personalized clinical algorithms.