Impaired Angiogenesis and Inflammation in Preeclampsia: A Review

Abstract

One of the key mechanisms of preeclampsia pathogenesis is an increase in the level of soluble Fms -like tyrosine kinase receptor 1 (sFlt-1) and soluble endoglin (sEng), which block the action of VEGF and PlGF, which are necessary for normal angiogenesis. This violation of vascular tone and deterioration of the blood supply to the placenta leads to hypoxia, inflammation and the development of complications. Elevated sFlt-1 and sEng levels are not only important biomarkers of preeclampsia but may also be targets for new therapeutic strategies. These molecules affect vascular dysfunction and inflammation, enhancing pathological processes that contribute to disease progression. Impaired angiogenesis also activates inflammatory cytokines that increase vascular permeability and contribute to the development of eclampsia and other severe forms of preeclampsia. This review aims to explore the role of impaired angiogenesis and inflammation in the pathogenesis of preeclampsia, highlighting potential therapeutic targets (sFlt-1 and sEng) for restoring angiogenic balance and improving maternal and fetal outcomes. Antiangiogenic factors such as sFlt-1 and sEng play a significant role, disrupting normal angiogenesis and placental blood supply. These processes form a vicious circle of vascular dysfunction, hypoxia and systemic inflammation, leading to severe pregnancy complications: intrauterine growth retardation, premature birth, HELLP syndrome, eclampsia and organ failure. A deeper understanding of the molecular and cellular mechanisms of hypertension pathogenesis during pregnancy allows not only to improve diagnostics and prognosis, but also to develop new targeted therapeutic strategies. In the future, therapy blocking the actions of sFlt-1 and sEng may become an effective treatment for preeclampsia, improving the prognosis for both mother and fetus.