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Miyoshi et al. show that silencing SMAD3 in iPSC-derived epicardial cells promotes epithelial-to-mesenchymal transition (EMT) toward the cardiac pericyte lineage with pro-angiogenic potential. SMAD3-downregulated epicardial cells cooperate with endothelial cells to enhance angiogenesis. Furthermore, these SMAD3-downregulated epicardial cells secrete more VEGFA and promote the proliferation of iPSC-derived cardiomyocytes in a paracrine manner.
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