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. 2015 Dec 31;6(12):e2033. doi: 10.1038/cddis.2015.370

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Copyright © 2015 Macmillan Publishers Limited

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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Schematic representation of the pathway involving NPR-C, Egr-1, miR199a-3p and miR199a-5p on ApoE modulation upon CC2238/αANP exposure in VSMCs. The positive effects of ApoE supplementation to VSMCs, despite CC2238/αANP exposure, support the strong contribution of this pathway into promotion of vascular damage through the final ApoE downregulation. C2238/αANP, variant αANP; NPR-C, type C natriuretic peptide receptor; ROS, reactive oxygen species; Egr-1, early growth response protein-1; miR199a, microRNA199a; CREG, cellular repressor of E1A-stimulated gene; JNK, c-Jun N-terminal kinase