Hypothetical framework for the pathogenesis of pre-eclampsia. Placental dysfunction triggered by poorly understood mechanisms—including genetic, immunologic, and environmental—plays an early and primary role in the development of pre-eclampsia. Placental dysfunction leads to aberrant production of antiangiogenic factors (soluble fms-like tyrosine kinase 1 and soluble endoglin), contributing to systemic endothelial cell dysfunction. Endothelial dysfunction, in turn, results in the systemic manifestations of pre-eclampsia.
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