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Nat. Rev. Cardiol. doi:10.1038/nrcardio.2017.103 Figure 7 Proposed mechanisms of arrhythmogenic cardiomyopathy and Brugada syndrome Figure 7 | Proposed mechanisms of arrhythmogenic cardiomyopathy and Brugada syndrome. Desmosomal mutations trigger fibrofatty tissue replacement via modulation of the transforming growth factor (TGF)-β1/p38 mitogen-activated protein kinase (MAPK)113, Hippo97 and Wnt/β-catenin signalling pathways105 (Fig. 4). In addition, adhesion defects induce apoptosis in cardiomyocytes; together these processes contribute to ventricular remodelling, which initially affects the right ventricular outflow tract (RVOT)8. Changes in cardiac tissue prompt monomorphic ventricular arrhythmias by a re-entry mechanism. By contrast, defects in Nav1.5 or associated proteins (such as plakophilin 2; PKP2) promote loss-of-function of the channel, inducing depolarization–repolarization defects. These abnormalities might participate in RVOT remodelling by affecting the function of cell-adhesion molecules (such as cadherin 2)18,91. According to repolarization and depolarization hypotheses, ST-segment elevation on the right precordial leads of the electrocardiogram is a consequence of electrical defects in the RVOT9, whereas structural remodelling in the RVOT contributes to those abnormalities in Brugada syndrome (BrS)12. Remodelling of the RVOT is a mechanism common to the pathogenesis of both arrhythmogenic cardiomyopathy (ACM) and BrS. Moncayo-Arlandi, J. & Brugada, R. (2017) Unmasking the molecular link between arrhythmogenic cardiomyopathy and Brugada syndrome Nat. Rev. Cardiol. doi:10.1038/nrcardio.2017.103