Key result
Combined genetic augmentation of creatine and creatine kinase in mice failed to rescue cardiac hypertrophy and contractile dysfunction due to downregulation of CK activity.
Population
CrT-OE, CKM-OE, double transgenic (dTg), and wildtype mice
Comparison
CrT and CKM overexpression vs wildtype
Design
Preclinical animal study across two experimental lines
Authors
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Excessive myocardial creatine may promote hypertrophy and dysfunction; leaves open creatine kinase modulation as a therapeutic target in cardiomyopathy.
In a mouse model, very high myocardial creatine levels cause hypertrophy and contractile dysfunction that cannot be rescued by concurrent creatine kinase overexpression due to enzyme downregulation.
Zervou et al. (2024) studied Cardiac hypertrophy and dysfunction. Combined overexpression of creatine transporter (CrT) and muscle isoform of creatine kinase (CKM) vs. Wildtype was evaluated on Cardiac function and hypertrophy. Combined genetic augmentation of creatine and creatine kinase in mice failed to rescue cardiac hypertrophy and contractile dysfunction due to downregulation of CK activity.
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