Abstract:Background:
Recent evidence demonstrates that not only NFAT, but also calcineurin is translocated into the nucleus upon hypertrophic stimulation. Previously it was also demonstrated that calpain-mediated degradation caused a constitutive active calcineurin. We hypothesised that nuclear calcineurin is an intranuclear Ca
2+
sensor hypertrophied myocardium and that inhibition of nuclear translocation of calcineurin is a therapeutic strategy to prevent hypertrophy.
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