Molecular Development of Placenta and Its Relationship with Preeclampsia and Fetal Growth Restriction

Abstract

Preeclampsia (PE) is the leading causes of maternal death worldwide as well as a significant cause of fetal morbidity and mortality, including fetal growth restriction (FGR). The concept that PE and FGR shared a common etiology is widely accepted, i.e., the maladaptive response to the impaired placentation. Normal placentation is the result of dynamic integration of cell proliferation, differentiation, and migration, in which trophoblast cells play a crucial role. Impaired trophoblast invasion into the maternal decidua leads to a decrease in uteroplacental blood flow and changes in intervillous hemodynamic. The dynamic interaction of these process with maladaptive decidual immune response, impaired cytokines and angiogenic factors regulation, and oxidative stress will lead into the clinical manifestation of PE and/or FGR.