Cardiomyocytes and stromal cells cross-talk influences the pathogenesis of arrhythmogenic cardiomyopathy: a multi-level analysis uncovers DLK1-NOTCH pathway role in fibro-adipose remodeling

Different cell types individually contribute to set the Arrhythmogenic Cardiomyopathy (ACM) phenotype with either functional abnormalities (cardiomyocytes; CM) or fibro-fatty substitution (cardiac mesenchymal stromal cells; cMSC). The relative contribution of the CM and cMSC derangements to determine disease evolution and electrical instability is still poorly understood. Here we showed that a patient-specific multicellular cardiac system, which models the functional interaction between CM and cMSC, provides insight into the relative contribution of different cell types to ACM phenotypes.