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. 2022 Mar 16;19(9):593–606. doi: 10.1038/s41569-022-00679-9

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© Springer Nature Limited 2022

This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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Fig. 5 — Epicardial adipose tissue (EAT) can affect heart function in the setting of heart failure via inflammation, fibrosis and neural dysregulation as observed in coronary artery disease and atrial fibrillation. However, several specific mechanisms link EAT with heart failure. The EAT proteome can contribute to the pathogenesis of heart failure through the paracrine secretion of profibrotic factors, such as α1-antichymotrypsin (ACT; also known as serpin A3) and matrix metalloproteinase 14 (MMP14), inflammatory markers, such as p53, and free fatty acids (FFAs). Large and fibrotic EAT can also exert mechanical effects on both diastolic and systolic function. EAT can also be involved in the pathogenesis of heart failure through neurohormonal mechanisms. The increased catecholamine biosynthetic activity of EAT can increase noradrenaline accumulation in the myocardium and worsen systolic performance. ECM, extracellular matrix.