1. Unless provided in the caption above, the following copyright applies to the content of this slide: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) For permissions please article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (
Eur Heart J, Volume 40, Issue 12, 21 March 2019, Pages 945–948,
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2. Figure 1 In normal heart, Dlk1 expression is high in cardiomyocytes (CM) leading to increased secretion of miR
Figure 1 In normal heart, Dlk1 expression is high in cardiomyocytes (CM) leading to increased secretion of miR-370 likely via exosomes. miR-370 acts on cardiac fibroblasts (CF) to block TGFβ signalling and transdifferentiation of myofibroblasts (MyFB) and fibrosis. However, under stress condition (i.e. myocardial infarction), Dlk1 expression is suppressed leading to downregulation of miR-370, stimulation of TGFβ signalling, and activation of myFB and induction of fibrosis and heart failure (from Rodriguez P, Sassi Y, Troncone L, Benard L, Ishikawa K, Gordon RE, Lamas S, Laborda J, Hajjar RJ, Lebeche D. Deletion of delta-like 1 homologue accelerates fibroblast–myofibroblast differentiation and induces myocardial fibrosis. See pages 967–978).
Unless provided in the caption above, the following copyright applies to the content of this slide: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) For permissions please article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (
Eur Heart J, Volume 40, Issue 12, 21 March 2019, Pages 945–948,
The content of this slide may be subject to copyright: please see the slide notes for details.