Abstract
Background: Arrhythmogenic cardiomyopathy (ACM) is an inherited disease mainly caused by desmosomal gene mutations and characterized by myocardial loss, replacement with fibro-fatty tissue, arrhythmias and sudden cardiac death. To date, it is unclear which cell type and molecular mechanisms contribute to the fibro-fatty phenotype. The epicardium is the outer mesothelial layer of the heart which has the capacity to undergo epithelial-to-mesenchymal transition and differentiate into various cardiac cell types. The aim of this study is to investigate whether epicardial cells (ECs) contribute to the excess fibro-fatty infiltration seen in ACM patients.
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