Abstract
Decidual vasculopathy is commonly associated with preeclampsia and develops in the late pregnancy in the uterine spiral arteries, which were previously remodeled by the extravillous trophoblasts. In normal early pregnancy, trophoblasts invade into the spiral artery, leading to vascular transformation, and this transformation is found to be associated with phenotypic switch of the endovascular trophoblasts to express CD56, a maternal protein likely from the natural killer (NK) cells. These endovascular trophoblasts are diminished at term. The decidual vessels are also returned to near normal at the delivery. Both the uterus and the uterine spiral arteries undergo involution after delivery. In preeclampsia, the endovascular trophoblasts are present within the vessel wall associated with the persistence of switched phenotype similar to those seen in the early implantation. The persistence of the endovascular trophoblasts in decidual vasculopathy indicates a failure to return to normal vessels in preeclampsia, thus suggesting a potential mechanism of pathogenesis. NK cells seem critical not only for early implantation and spiral artery remodeling but also for the development of decidual vasculopathy in preeclampsia. In this short review, some critical aspects of decidual vasculopathy in normal pregnancy and preeclampsia are reexamined and a new hypothesis is proposed.