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. Author manuscript; available in PMC: 2020 May 1.
Published in final edited form as: Nat Rev Nephrol. 2019 May;15(5):275–289. doi: 10.1038/s41581-019-0119-6

Fig. 4 ∣. The role of sFLT1 in endothelial dysfunction in pre-eclampsia.

Fig. 4 ∣

a ∣ During normal pregnancy, vascular homeostasis is maintained by physiological levels of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) signalling in the vasculature by binding to its receptor fms-like tyrosine kinase 1 (FLT1) and other signalling receptors. b ∣ In pre-eclampsia, excess soluble FLT1 (sFLT1) is secreted by the placenta and binds local and circulating VEGF and PlGF, resulting in inhibition of VEGF and PlGF signalling in the vasculature. This inhibition results in endothelial cell dysfunction, including reduced production of prostacyclin and nitric oxide and the release of procoagulant proteins.