Figure 1 Pre-eclampsia prevents VEGF signalling in endothelial cells

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Figure 1 Pre-eclampsia prevents VEGF signalling in endothelial cells Figure 1 | Pre-eclampsia prevents VEGF signalling in endothelial cells. The binding of vascular endothelial growth factor (VEGF) to the VEGF receptors FMS-like tyrosine kinase 1 (FLT1) and fetal liver kinase 1 (FLK1) initiates signalling that leads to the production of nitric oxide (NO) by endothelial cells, which is required for vasodilation (not shown). During pre-eclampsia, the levels of a soluble isoform of FLT1 (sFLT1) — a decoy VEGF receptor that reduces circulating levels of VEGF — are elevated. Increased levels of sFLT1 result in a reduction in canonical VEGF signalling in the vascular endothelium, leading to aberrant vasoconstriction through decreased NO production and increased production of vasoconstrictors, such as endothelin 1. George, E. M. & Granger, J. P. (2017) A new genetic clue to unravel the origins of pre-eclampsia Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.116