Abstract
The two central pathophysiological themes of preeclampsia are: (1) placental trophoblast dysfunction; and (2) endothelial dysfunction within the maternal systemic vasculature. No single factor has been identified as the cause of preeclampsia, however, substantial evidence suggests that the increased oxidative stress, production of vasoconstrictor agents, altered placental cytokine generation, and the formation of other toxic compounds produced by the placenta promote several forms of endothelial dysfunction in preeclampsia. The effects of such placental factors on maternal vascular cells (e.g. endothelial cells, neutrophils and platelets), combined with pre-existing maternal risk factors (vascular, renal, and metabolic diseases), with immune abnormalities and genetic factors pose substantial risks for developing this disorder during pregnancy. While placental dysfunction may not be the sole cause of preeclampsia, placental dysfunction may trigger, or significantly contribute to the vascular complications associated with preeclampsia.
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