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. 2021 Feb 2;30(2):178–186. doi: 10.1089/jwh.2020.8852

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© Jasmina Varagic et al. 2021; Published by Mary Ann Liebert, Inc.

This Open Access article is distributed under the terms of the Creative Commons Attribution Noncommercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are cited.

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FIG. 1. — Signaling pathways, potential biomarkers, and therapeutic targets in PE. Placental ischemia-derived imbalance in proangiogenic (VEGF and PlGF) and antiangiogenic (sFlt-1 and sEng) factors, oxidative stress, and inflammation led to systemic vascular dysfunction reflected in hypertension and proteinuria in PE. Potential targeted interventions include blockade, removal, or competitive binding of sFlt-1 or supplementation of recombinant isoforms of proangiogenic factors. AT1-AA, AT1 receptor autoantibodies; PE, preeclampsia; PlGF, placental growth factor; sEng, soluble endoglin; sFlt-1, soluble fms-like tyrosine kinase-1; VEGF, vascular endothelial growth factor.