Abstract: Preeclampsia is a pregnancy specific complication which is characterized by systemic endothelial cell activation and exaggerated inflammatory response. Although the pathogenesis of preeclampsia is unclear，it is well recognized that placental factor(s) and maternal factor(s) contribute to the pathogenesis of preeclampsia. Trophoblastic debris shed from placenta is one of the possible placental factors. During the pregnancy, trophoblastic debris is shed into the maternal blood to become trapped against the maternal pulmonary endothelium as early as 6 weeks of gestation in an apoptosis form. Trophoblastic debris was reported to be involved in the pathogenesis of preeclampsia in 1893. The increased amount of trophoblastic debris is seen in preeclampsia. Recent study showed that phagocytosis of necrotic trophoblastic debris results in endothelial cell activation that seen in preeclampsia. There are many potential factors that could switch apoptotic trophoblastic debris into necrotic trophoblastic debris. Of them, antiphospholid antibodies, inflammatory cytokines like IL-6, TGF-β1 and failure of spiral artery transformation play an important role on it. To date even there is no effective treatment on preeclampsia, calcium and vitamin C supplementation may reduce the risk for developing preeclampsia through preventing endothelial cell activation induced by phagocytosis of necrotic trophoblastic debris.

Key words: Trophoblasts, Pre-eclampsia, Endothelial cells