Despite recent progress in developing treatments for dilated cardiomyopathy (DCM), mortality remains high. Given that insulin-like growth factor-1 (IGF1) improves myocardiocyte function in other pathological settings, Touvron et al. investigated whether IGF1 would also be beneficial in an established mouse model of DCM. The model involves cardiac-specific inducible knockout of serum response factor (Srf), encoding a transcription factor important for heart development and function; fatal DCM occurs within 10 weeks of inducing Srf deletion. Crossing these to mice that overexpress IGF1 in cardiomyocytes resulted in a strain that showed delayed DCM, better cardiac function and longer lifespan after Srf deletion. Overexpression of IGF1 also markedly reduced cardiac fibrosis and inflammation, partly by counteracting the increased expression of connective tissue growth factor (CTGF) caused by Srf deletion. These results further understanding of how SRF contributes to heart failure and suggest that IGF1 might be a promising therapeutic. Page 481

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