Soluble Fms-like tyrosine kinase 1 and endothelial dysfunction in the pathogenesis of preeclampsia.
Preeclampsia, a pregnancy-specific syndrome of hypertension and proteinuria, is characterized by defective placental vasculogenesis and widespread maternal endothelial dysfunction. Although the manifestations of preeclampsia are primarily maternal, the burden of morbidity and mortality is often on the neonate, since the only effective treatment-delivery of the fetus and placenta-often results in iatrogenic prematurity. In this review, we summarize recent advances in our understanding of the pathophysiology of preeclampsia, including normal and aberrant placental vascular development and evidence for endothelial dysfunction. We describe recent evidence that supports a novel mechanism in which a maladaptive shift in placental production of angiogenic factors such as soluble fms-like tyrosine kinase 1 (a circulating antiangiogenic protein) may play an important role in the pathogenesis of preeclampsia.
Maynard
Sharon E
SE
Department of Medicine, University of Massachusetts Medical School, Worcester 01655, USA.
Venkatesha
Shivalingappa
S
Thadhani
Ravi
R
Karumanchi
S Ananth
SA
D004730:Endothelium, Vascular / Q000473:pathology*; D005260:Female; D006801:Humans; D018919:Neovascularization, Physiologic; D010920:Placenta / Q000378:metabolism / Q000473:pathology; D011225:Pre-Eclampsia / Q000378:metabolism* / Q000473:pathology*; D011247:Pregnancy; D017434:Protein Structure, Tertiary; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000378:metabolism / Q000502:physiology*
D040281:Vascular Endothelial Growth Factor Receptor-1