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Transgenic (Tg) overexpression of a poison Mybpc340kDa peptide fragment in a cardiomyocyte (CM)-specific manner leads to hypertrophic cardiomyopathy and heart failure, characterized by severe fibrosis. Myofibroblast (MyoFB)-specific deletion of Tgfbr2 decreases fibrosis and improves cardiac function and survival, despite continued presence of the toxic peptide. FB=Fibroblasts. MCM=Mer-Cre-Mer.
