Key result
Acute expression of the R9C-PLB mutation exerted a positively inotropic and lusitropic effect in cardiomyocytes, but impaired frequency potentiation and blunted β-adrenergic responsiveness.
Population
Adult cardiomyocytes and live cells
Design
Preclinical
Authors
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Acute R9C-PLB effects on calcium handling in rodent cardiomyocytes are clarified; leaves open translation to human cardiomyopathy therapies.
The R9C-PLB mutation acutely increases contractility but impairs frequency potentiation and β-adrenergic responsiveness, suggesting a mechanism for progression to heart failure.
Abrol et al. (2015) studied Cardiomyopathy. Acute expression of R9C-PLB mutation was evaluated on Cardiomyocyte calcium kinetics, contractility, PLB oligomerization, and PLB-SERCA binding. Acute expression of the R9C-PLB mutation exerted a positively inotropic and lusitropic effect in cardiomyocytes, but impaired frequency potentiation and blunted β-adrenergic responsiveness.
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