Why the study?
Does genetic deletion of Calstabin2 accelerate age-related cardiac dysfunction in mice?
Population
Calstabin2 knockout (KO) and control wild-type (WT) mice
Comparison
Genetic deletion of Calstabin2 vs Wild-type (WT) littermates
Design
Preclinical
Authors
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Calstabin2 deletion accelerates cardiac aging in mice; leaves open whether pathway targeting could mitigate human age-related HF.
Does genetic deletion of Calstabin2 accelerate age-related cardiac dysfunction in mice?
Calstabin2 is a key modulator of cardiac aging, with its deletion leading to impaired cardiac function and accelerated aging phenotypes via the AKT/mTOR pathway.
Yuan et al. (2014) studied this question.
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