Abstract
Preeclampsia affects about 3–8% of all pregnancies. It represents a complex and multifaceted syndrome with at least several potential pathways leading to the development of disease. The main dogma in preeclampsia is the two-stage model of disease. Stage 1 (placental stage) takes place in early pregnancy and is thought to be impaired placentation due to inadequate trophoblastic invasion of the maternal spiral arteries that leads to reduced placental perfusion and release of numerous biological factors causing endothelial damage and development of acute maternal syndrome with systemic multiorgan failure (stage 2—the onset of maternal clinical symptoms, maternal stage). Recently, in the light of the vast body of evidence, two-stage model of preeclampsia has been updated with a few novel pathways leading to clinical manifestation in the second part of pregnancy. This paper reviews current state of knowledge about pathophysiology of preeclampsia and places particular focus on the recent advances in understanding of uterine artery remodeling alterations, as well as the role of microRNAs in preeclampsia.
Highlights
Preeclampsia (PE) affects about 3–8% of all pregnancies
Because miRNA-218-5p is downregulated in preeclamptic placentas and serum transforming growth factor β2 (TGF-β2) is increased in PE patients, the authors of this study suggested that downregulation of miRNA-218-5p may contribute to the development of PE [73]
This review summarizes current knowledge about factors and processes involved in the development of PE
Summary
Preeclampsia (PE) affects about 3–8% of all pregnancies. It is the main cause of perinatal morbidity and mortality in developed countries, responsible for about 16–18% of maternal deaths and about 40% of fetal and neonatal deaths [1]. PE represents a complex and multifaceted syndrome with at least several potential pathways leading to the development of disease It is a systemic condition with global endothelial dysfunction and multiorgan failure affecting both maternal and fetal health. PE have four-fold increased risk of heart failure, two-fold increased risk of coronary artery disease, two-fold increased risk of stroke, and two-fold increased risk of cardiovascular death later in life [5,6] They have increased risk of developing microalbuminuria and end-stage renal disease in the future [7,8,9]. Some points are still missing, and termination of pregnancy remains as the only effective therapy [2,11,12] This narrative review aims to summarize recent advances in understanding of PE pathophysiology with particular emphasis on defective uterine artery remodeling and the role of microRNAs
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