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

<div class="floats-full-page floats-full-page-figure"><h2>Figure 2</h2><div class="floats-full-page-caption"><table>Proposed molecular mechanism underlying TGF<i>β</i>3-induced myocardial fibrofatty infiltration. Smad signaling is activated by TGF<i>β</i> receptors and induces fibrogenesis. Simultaneously, TGF<i>β</i> signaling enhances Wnt/<i>β</i> catenin signaling, whereas Smad proteins inhibit <i>β</i>-catenin altered gene expression. This augments fibrosis or hinders myogenesis, respectively. The net result is increased fibrofatty infiltration in cardiac tissue.</table></div><div class="floats-full-page-content"><table class="table-group" width="800px"><tr class="fig-image"><td><img alt="460805.fig.002" src="https://static-01.hindawi.com/articles/gri/volume-2013/460805/figures/460805.fig.002.jpg" /></td></tr></table></div></div>

Figure 2 | Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy Type 1: A Light on Molecular Mechanisms

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Figure 2: Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy Type 1: A Light on Molecular Mechanisms

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Figure 2

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<p><em>Genetics Research International</em> publishes original research articles and review articles in all areas of genetics and genomics. The journal focuses on articles bearing on heredity, biochemistry, and molecular biology, as well as clinical findings.</p>


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