An unexpected finding here is that the SERCA2-KO hearts retained a highly significant diastolic functional reserve upon β-adrenergic stimulation and not different from that of control SERCA2 replete hearts. β-Adrenergic stimulation is well known to markedly enhance myocardial contractile performance via several key phosphoproteins.
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Myofilament-based physiological regulatory compensation preserves diastolic function in failing hearts with severe Ca2+ handling deficits.
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