Molecular mechanisms of preeclampsia

In recent years, studies have been conducted indicating an association between preeclampsia (PE) and an imbalance of angiogenic factors. This imbalance leads to disruption of endothelial function, resulting in PE. Preeclampsia is associated with problems of placental cytotrophoblast invasion and spiral artery remodeling. This impedes normal perfusion of the placenta, in response to which the body produces inflammatory and antiangiogenic factors, which are present in large quantities in the maternal blood during PE. Factors such as placental growth factor (PGF), soluble fms-like tyrosine kinase-1 (sFlt-1), and placental protein 13 are thought to be part of this process. They can damage the mother’s vascular walls, causing endothelial dysfunction, increased blood pressure and, in some cases, organ death and maternal death. Determining the level of placental biomarkers facilitates the timely diagnosis of preeclampsia and the prescription of appropriate treatment. This information helps us better understand the mechanisms behind the development of preeclampsia, but it is important to remember that it is a complex condition that requires medical intervention and monitoring.