Increased maternal sFlt-1 levels decrease circulating free
PlGF and VEGF concentrations leading to endothelial dysfunction.
The second antiangiogenic protein, soluble endoglin
(sEng) may impair the binding of transforming growth factor-1
to endothelial receptors, thereby decreasing endothelial
nitric oxide– dependent vasodilatation. Simultaneous introduction
of adenoviruses encoding both sFlt-1 and sEng into pregnant
rats produces severe hypertension, heavy proteinuria, elevated
liver enzyme levels, and circulating schistocytes—in
essence creating a powerful rodent model that simulates most
of the protean manifestations of preeclampsia in humans and
has obvious implications for the