Key result
Induction of constitutively active FGFR1 in adult mouse cardiomyocytes rapidly increased cardiac contractility and resulted in significant concentric hypertrophy with preserved systolic function.
Why the study?
Does constitutively active FGFR1 signaling increase contractility and induce hypertrophic cardiomyopathy in adult mouse cardiomyocytes?
Does constitutively active FGFR1 signaling increase contractility and induce hypertrophic cardiomyopathy in adult mouse cardiomyocytes?
Absolute Event Rate: 5.3% vs 4.2%
p-value: p=0.02
Constitutive activation of FGFR1 in adult cardiomyocytes is sufficient to increase contractility and induce a hypertrophic cardiomyopathy phenotype with dynamic outflow tract obstruction.
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Should not alter clinical practice; leaves open FGFR1 as a target in human hypertrophic remodeling.
Cilvik et al. (2013) studied Hypertrophic Cardiomyopathy. Constitutively active FGFR1 induction vs. Control mice (single transgenic or wild-type) was evaluated on Left ventricular mass index (mg/g) at 1 week (p=0.02). Induction of constitutively active FGFR1 in adult mouse cardiomyocytes rapidly increased cardiac contractility and resulted in significant concentric hypertrophy with preserved systolic function.
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