Why the study?
Mitochondrial creatine kinase is down-regulated in chronic heart failure and may contribute to disease progression, leading researchers to test if its cardiomyocyte-specific overexpression would preserve cardiac function.
Does cardiomyocyte-specific overexpression of Mt-CK preserve cardiac function and energetics in a murine model of pressure overload-induced chronic heart failure?
Population
Male Mt-CK overexpressing mice and WT littermates
Comparison
TAC vs sham surgery in Mt-CK overexpressing mice vs WT littermates
Design
Animal experimental study
Follow-up
6 weeks
Authors
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Preserves energetics without improving function or remodeling in pressure-overload mice; leaves open therapeutic translation of Mt-CK overexpression.
Does cardiomyocyte-specific overexpression of Mt-CK preserve cardiac function and energetics in a murine model of pressure overload-induced chronic heart failure?
Overexpression of Mt-CK in mice preserves cardiac energetics during pressure overload but does not prevent the development of chronic heart failure or improve LV function.
Cao et al. (2020) studied this question.
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