Why the study?
Does constitutively active AMPK alter action potential duration and sodium channel currents in ventricular myocytes?
Population
Rat ventricular myocytes and a mammalian cell line expressing human cardiac sodium channel hH1
Comparison
Expression of a truncated constitutively active… vs null
Design
Preclinical
Authors
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May link AMPK dysregulation to arrhythmogenesis in PRKAG2 cardiomyopathy; hypothesis-generating and requires human validation.
Does constitutively active AMPK alter action potential duration and sodium channel currents in ventricular myocytes?
Constitutively active AMPK prolongs action potential duration and alters sodium channel kinetics, providing a potential mechanism for arrhythmogenesis in patients with PRKAG2 mutations.
Light et al. (2003) studied this question.
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