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Abnormal trophoblastic invasion and impaired placentation have a crucial role in the etiopathogenesis of preeclampsia (PrE). Trophoblastic cells are involved in invading the maternal decidua and remodelling of the spiral arteries with matrix metalloproteinase-14 (MMP-14). MMP-14 cleavage of endoglin releases its extracellular region, the soluble form of endoglin (s-ENG), into the maternal circulation. In PrE, there is a relationship between endothelial dysfunction and s-ENG concentration. The aim was to determine and compare the serum leve
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