Key result
In mice with conditional SERCA2 knockout, sodium accumulation impaired NCX-mediated calcium extrusion, promoting diastolic dysfunction in end-stage heart failure.
In a mouse model of SERCA2 knockout, sodium accumulation contributes significantly to diastolic dysfunction by impairing NCX-mediated calcium extrusion.
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Time-dependent HF onset after SERCA deletion in mice leaves open compensatory mechanisms; hypothesis-generating for Ca2+ therapies.
Louch et al. (2009) studied Heart failure. Cardiomyocyte-specific excision of the SERCA gene was evaluated on Cardiac function, cardiomyocyte contraction and relaxation, and Ca(2+) transients. In mice with conditional SERCA2 knockout, sodium accumulation impaired NCX-mediated calcium extrusion, promoting diastolic dysfunction in end-stage heart failure.
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