Before revision:  This work, together with the recent study by Hannanta-anan and Chow, suggests a ]  plausible mechanism for IP3-dependent hypertrophic signalling in cardiomyocytes.
After revision:  This work, together with the recent study by Hannanta-anan and Chow, suggests a ] is elevated, across a broad range of parameter values and IP3 concentrations. When coupled to a model of downstream transcription factor (NFAT) activation, we demonstrate that there is a high correspondence between the Ca transient duty cycle and the proportion of activated NFAT in the nucleus. These findings suggest increased cytosolic Ca2+ duty cycle as a plausible mechanism for IP3-dependent hypertrophic signalling in cardiomyocytes.