Key result
KCNE1 was 4- to 10-fold overexpressed in TRalpha1-deficient mice, and its transgenic overexpression caused lower heart rate and prolonged QT(end) time, explaining bradycardia in hypothyroid states.
Why the study?
Does TRalpha1 deficiency or KCNE1 overexpression alter action potential duration and heart rate in mouse ventricular myocytes?
Population
TR-deficient mice, KCNE1-overexpressing transgenic mice, their respective wildtype mice, and Chinese hamster…
Comparison
Genetic modification vs Respective wildtype (wt) mice
Design
Preclinical
Authors
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May mediate hypothyroid bradycardia via KCNE1 in mice; leaves open human translation and therapeutic relevance.
Does TRalpha1 deficiency or KCNE1 overexpression alter action potential duration and heart rate in mouse ventricular myocytes?
The bradycardia and prolonged QT interval seen in hypothyroid states may be mediated by decreased TRalpha1-dependent repression of KCNE1 expression, leading to altered K+ channel function.
Mansén et al. (2009) studied Hypothyroid states. KCNE1 overexpression vs. Wildtype mice was evaluated on Heart rate and QT(end) time. KCNE1 was 4- to 10-fold overexpressed in TRalpha1-deficient mice, and its transgenic overexpression caused lower heart rate and prolonged QT(end) time, explaining bradycardia in hypothyroid states.
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