Key result
Postnatal deletion of Foxm1 from cardiomyocytes in mice resulted in normal early cardiac development but caused late-onset cardiac hypertrophy and fibrosis without exacerbating pressure overload-induced remodeling.
Why the study?
Does postnatal ablation of Foxm1 from cardiomyocytes cause cardiac hypertrophy and fibrosis or exacerbate pressure overload-induced cardiac remodeling in mice?
Population
Mice with postnatal cardiomyocyte-specific deletion of Foxm1 (αMHC-Cre/Foxm1fl/fl) and control Foxm1fl/fl mice
Comparison
Postnatal ablation of Foxm1 from cardiomyocytes… vs Control mice with intact Foxm1 (Foxm1fl/fl)
Design
Preclinical
Follow-up
Up to 16 months of age; 18 weeks after aortic banding
Authors
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No immediate clinical implications from this mouse model; leaves open Foxm1 as a regulator of age-related cardiac changes.
Does postnatal ablation of Foxm1 from cardiomyocytes cause cardiac hypertrophy and fibrosis or exacerbate pressure overload-induced cardiac remodeling in mice?
Foxm1 regulates genes critical for age-induced cardiomyocyte hypertrophy and cardiac fibrosis, but is dispensable for pressure overload-induced remodeling.
Bolte et al. (2012) studied Cardiac hypertrophy and fibrosis. Postnatal ablation of Foxm1 from cardiomyocytes vs. Foxm1fl/fl control mice was evaluated on Cardiac morphology, function, and development of hypertrophy/fibrosis. Postnatal deletion of Foxm1 from cardiomyocytes in mice resulted in normal early cardiac development but caused late-onset cardiac hypertrophy and fibrosis without exacerbating pressure overload-induced remodeling.
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