Frank T. Spradley

TL;DR: The placenta plays a central role in the pathogenesis of pre-eclampsia and reduced uteroplacental perfusion, which develops as a result of abnormal cytotrophoblast invasion of spiral arterioles, triggers the cascade of events leading to the maternal disorder as discussed by the authors.

TL;DR: The novel finding that recombinant human PlGF abolishes placental ischemia-induced hypertension, without major adverse consequences, suggests a strong therapeutic potential for this growth factor in preeclampsia.

TL;DR: Recent studies that link placental ischemia, endothelial and vascular dysfunction, and hypertension in preeclampsia are reviewed to review and suggest markers that could prove useful in the diagnosis of the disorder.

TL;DR: The concept that obesity and metabolic factors like lipids, insulin, glucose, and leptin affect placental function and increase the risk for developing hypertension in pregnancy is summarized by reducing placental perfusion; enhancing placental release of soluble factors; and by increasing the sensitivity of the maternal vasculature to placental ischemia-induced soluble factors.

TL;DR: It is speculated that these factors potentiate the anti-angiogenic and proinflammatory mechanisms of placental ischemia-induced vascular dysfunction thereby contributing to the increasing incidence of PE.