Preeclampsia is a human disease, usually occurring during the third trimester of pregnancy. The underlying pathogenetic mechanisms of preeclampsia are much debated. Current hypotheses include placental dysfunction, inflammatory disease, genetic predisposition and immune maladaptation. Recent studies highlight the role of vascular-mediated factors in the pathophysiology of preeclampsia and allow new hopes for screening and therapeutic approaches. This article describes pathophysiological mechanisms involved in the defective uteroplacental vascularization leading to placental and endothelial dysfunction.