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. 2017 Feb 2;8(2):e2590. doi: 10.1038/cddis.2016.483

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Copyright © 2017 The Author(s)

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Putative model of CER-mediated necroptosis and its role in the pathogenesis of preeclampsia. CER overload in preeclamptic placentae primes RIP1/RIP3 necrosome assembly. Conditions of reduced caspase-8 activity, as demonstrated in E-PE, favor CER to cause MLKL phosphorylation and oligomerization at the cell membrane where it executes necroptosis by permeabilizing the membrane. Necroptotic cell death also prevents normal cytotrophoblast fusion that is required to replenish the syncytiotrophoblast layer, resulting in improper cell turnover