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. 2018 Aug 25;9:36. doi: 10.1186/s13293-018-0195-5

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — Contribution of sFlt-1 to the maternal syndrome of preeclampsia. In preeclampsia, it is believed that the maternal vasculature fails to remodel and provide adequate blood flow to the placenta, causing chronic ischemia. As a result, the placenta produces various factors, notably sFlt-1, which contribute to the maternal syndrome. sFlt-1 acts as a decoy receptor for VEGF and PlGF, causing decreased bioavailable VEGF protein. This leads to maternal vascular endothelial dysfunction, causing aberrant vasoconstriction, changes in renal function, and ultimately hypertension