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. 2020 Aug 30;9(2):363–376. doi: 10.1007/s40119-020-00199-y

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial 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-nc/4.0/.

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Fig. 2 — Schema representing the development of myocardial fibrosis and sites of action of potential therapeutic targets. RAAS renin–angiotensin–aldosterone system, TGFβ tissue growth factor-β, TNFα tumour necrosis factor-α, CTGF connective tissue growth factor, IL-11 interleukin-11, miRNA microRNA, MMP matrix metalloproteinases, Gal-3 galectin-3