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. 2022 Dec 28;24(3):261–275. doi: 10.1093/ehjci/jeac242

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© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Potential therapeutic targets in myocardial fibrosis. Relevant pathways involved in fibrosis formation include Angiotensin-II, transforming growth factor-β, and interleukin-11 making them key treatment targets. Other targets include the renin–angiotensin–aldosterone system, sympathetic and immune systems, endothelin 1, stem cell therapy, CAR-T therapy, and theranostic FAP inhibitor agents. AngII, angiotensin-II; ACE-i, angiotensin-converting-enzyme inhibitors; ARB, angiotensin receptor blocker; ARNI, angiotensin receptor-neprilysin inhibitor; AT1, Angiotensin receptor; CAR-T, chimeric antigen receptor-modified T cells; ET-1, endothelin-1; FAPI, fibroblast activation protein inhibitor; FAP, fibroblast activation protein; IL, interleukin; PDGF, platelet-derived growth factor; RAAS, renin–angiotensin–aldosterone system; SGLT2i, sodium-glucose cotransporter-2 inhibitor; TGF-β, transforming growth factor (beta).