Key result
TR alpha1 deficiency prolongs mouse cardiomyocyte action potentials by ~4 msec via accelerated K+ inactivation.
Why the study?
Does thyroid hormone receptor alpha1 deficiency alter depolarization-activated K+ currents and action potential duration in mouse ventricular cardiomyocytes?
Population
Ventricular heart cells isolated from mice lacking the thyroid hormone receptor alpha1 (TR alpha1)
Comparison
Thyroid hormone receptor alpha1 deficiency vs Wild-type cells
Design
Preclinical
Authors
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Should not inform clinical QT management; leaves open TRα1's role in human repolarization mechanisms.
Does thyroid hormone receptor alpha1 deficiency alter depolarization-activated K+ currents and action potential duration in mouse ventricular cardiomyocytes?
TR alpha1 deficiency accelerates the inactivation of voltage-dependent K+ outward currents and prolongs action potential duration in murine cardiomyocytes, providing a mechanistic basis for prolonged QT intervals.
Johansson et al. (2002) studied this question. Thyroid hormone receptor alpha1 (TR alpha1) deficiency vs. Wild-type cells was evaluated on Time- and voltage-dependent properties of depolarization-activated K+ currents and action potential duration. TR alpha1 deficiency in mouse cardiomyocytes accelerated the total inactivation time course of K+ outward currents and prolonged action potential duration by 3.6 msec compared with wild-type cells.
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