Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy Type 1: A Light on Molecular Mechanisms

Figure 2

Proposed molecular mechanism underlying TGFβ3-induced myocardial fibrofatty infiltration. Smad signaling is activated by TGFβ receptors and induces fibrogenesis. Simultaneously, TGFβ signaling enhances Wnt/β catenin signaling, whereas Smad proteins inhibit β-catenin altered gene expression. This augments fibrosis or hinders myogenesis, respectively. The net result is increased fibrofatty infiltration in cardiac tissue.