Preeclampsia still represents the leading cause of feto-maternal morbi-mortality in developed countries. The reason for the persistence of such gravity results to a large extent from the lack of clear knowledge concerning the pathophysiology of this disease and consequently the lack of adequate therapy apart from placental extraction. Preeclampsia is the clinical result of a generalized maternal systemic endothelial dysfunction secondary to an abnormal placental development. The close mechanisms of the abnormal placental development remain elusive. Currently, only epidemiologic risk factors and some immuno-genetic dysfunctions have been identified to favour abnormal placentation and preeclampsia. On the other hand, the identification of two circulating anti-angiogenic proteins, the soluble-fms-like tyrosine kinase-1 and the soluble endoglin, produced in excess by the placenta during the preeclampsia, allow us now to connect clearly abnormal placentation to an endothelial dysfunction. The excessive production of these two anti-angiogenic proteins induces an endothelial dysfunction by inhibiting circulating proangiogenic factors such as the placental growth factor, the vascular endothelial growth factor but also the transforming growth factor-beta. So far, numerous placental factors have been proposed, however none has been able to induce a real typical phenotype of preeclampsia. This discovery has two potential medical impacts. Firstly, the potential possibility, in the future, to measure these surrogate markers in the blood or urine to predict the onset of preeclampsia before its clinical manifestations. Secondly the theoretical possibility to reverse the angiogenic imbalance state of preeclamspsia and consequently to correct the maternal syndrome transiently by adding exogenous proangiogenic factor.