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. 2020 Aug 4;35(5):1025–1044. doi: 10.1007/s10557-020-07019-4

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Schematic overview highlighting key changes in DNA and RNA methylation in endothelial cells that occur in response to cardiac stress promoting endothelial dysfunction and pathological remodelling in the heart. Endothelial progenitor cells (EPCs); nitric oxide (NO); prostaglandins (PGI2); reactive oxygen species (ROS); DNA 5-methylcytosine (5MeC); 5-hydroxymethylcytosine (5hMeC); DNA methyltransferase (DNMT); methyl-CpG-binding domain protein 2 (MBD2); ten-eleven-translocation 2 enzyme (TET2); NOP2/Sun domain family member 2 (NSUN2); RNA 5-methylcytosine (m5C); N6-methyladenosine (m6A); methyltransferase like 3 (METTL3); methyltransferase like (METTL14); Wilms’ tumour-associated protein (WTAP); YTH N6-methyladenosine RNA binding protein 1 (YTHDF2)