Key result
Cardiac-specific overexpression of hMCIP1 significantly reduced cardiac hypertrophy induced by constitutively active calcineurin (heart weight/body weight ratio 5.69 vs 9.92 mg/g, p<0.01).
Why the study?
Does cardiac-specific overexpression of hMCIP1 inhibit cardiac hypertrophy in transgenic mice?
Does cardiac-specific overexpression of hMCIP1 inhibit cardiac hypertrophy in transgenic mice?
Absolute Event Rate: 5.69% vs 9.92%
p-value: p=<0.01
Cardiac-specific overexpression of hMCIP1 inhibits multiple forms of cardiac hypertrophy in vivo without apparent deleterious effects in normal hearts, suggesting a potential therapeutic target for preventing heart failure.
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Hypothesis-generating for MCIP1 as anti-hypertrophic target; leaves open translation to human heart failure prevention.
Rothermel et al. (2001) studied Cardiac hypertrophy (n=78). hMCIP1 overexpression (a-MHC-hMCIP1 transgene) vs. Wild-type littermates or a-MHC-CnA* transgenic mice was evaluated on Heart weight to body weight ratio (mg/g) in genetic model of cardiomyopathy (p=<0.01). Cardiac-specific overexpression of hMCIP1 significantly reduced cardiac hypertrophy induced by constitutively active calcineurin (heart weight/body weight ratio 5.69 vs 9.92 mg/g, p<0.01).
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