Preeclampsia is a systemic syndrome that occurs during pregnancy and is characterized by proteinuria and hypertension; it is accompanied by a substantial increase in maternal and perinatal morbidity and mortality rates. In preeclampsia, there is initially impaired cytotrophoblast invasion and then endothelial dysfunction in the mother and the fetus. In preeclampsia, there is also an increase in the synthesis of antiangiogenic growth factors, such as soluble fms-like tyrosine kinase and soluble endoglin. These factors migrate into the mother across the placenta and lead to endothelial dysfunction that manifests as hypertension, proteinuria, and other abnormalities. The molecular bases of placental damage are still unknown. In this case, hypoxia may play a significant role. Other factors, such as changes in the renin-angiotensin-aldosterone system, immune disadaptation, and genetic factors, are of defined value in the mechanisms of impaired placentation. Prospective studies of the blood and urine levels of pro- and antiangiogenic factors are required to develop informative markers for predicting preeclampsia and to elaborate new methods of its therapy.