Preeclampsia is a major cause of maternal, fetal and neonatal mortality worldwide. The etiology of preeclampsia is still unclear. Currently, the inadequate transformation of the smooth muscle cells of spiral arteries in the placental bed caused by an insufficient endovascular invasion of the trophoblast is considered to be the major reason for the development of preeclampsia. This insufficient invasion seems to lead to altered placental angiogenesis which thus has causal importance for the development of preeclampsia. Vascular endothelial growth factor (VEGF) and placental growth factor (PLGF) are the most important angiogenic factors with regulatory functions for placental vessel development. In preeclamptic pregnancies the expression of VEGF and PLGF was decreased. However, the expression of the corresponding receptor, the soluble fins-like tyrosine kinase receptor, which is considered to have anti-angiogenic properties, was elevated in preeclamptic pregnancies. CYR61 and NOV which belong to a group of proteins, the CCN-family, play also an important role in the regulation of placental angiogenesis. Recently, a decreased expression of both proteins in the placentae of preeclamptic women was detected. This review summarizes our current understanding of the role of angiogenic factors in the pathogenesis of preeclampsia.