Key result
Overexpression of the myocardial creatine transporter in mice led to left ventricular dilatation and reduced ejection fraction (49% vs 64% in wild-type controls; P=0.003).
Why the study?
Does overexpression of the myocardial creatine transporter affect cardiac function and energy metabolism in mice?
Population
Transgenic mouse lines overexpressing the myocardial creatine transporter and wild-type littermate controls
Comparison
Overexpression of the myocardial creatine… vs Wild-type (WT) littermate controls
Design
Preclinical
Authors
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Supranormal myocardial creatine may impair LV function in mice; leaves open effects of creatine supplementation in human heart disease.
Does overexpression of the myocardial creatine transporter affect cardiac function and energy metabolism in mice?
Absolute Event Rate: 49% vs 64%
p-value: p=0.003
Supranormal levels of myocardial creatine and phosphocreatine via creatine transporter overexpression lead to energetic impairment, LV hypertrophy, and dysfunction, cautioning against the uncritical use of creatine as a therapeutic agent in heart disease.
Wallis et al. (2005) studied Heart failure. Overexpression of the myocardial creatine transporter (CrT-OE) vs. Wild-type (WT) littermate controls was evaluated on Left ventricular ejection fraction (p=0.003). Overexpression of the myocardial creatine transporter in mice led to left ventricular dilatation and reduced ejection fraction (49% vs 64% in wild-type controls; P=0.003).
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