Key result
Thyroid hormone T3 up-regulated minK mRNA specifically in the rat atrium, which may contribute to the frequent occurrence of atrial fibrillation in hyperthyroidism.
Why the study?
Does triiodothyronine (T3) modulate the gene expression of voltage-gated potassium channels in adult rat hearts?
Population
Adult rats
Comparison
Triiodothyronine 25µg/100g body weight via… vs Control state
Design
Preclinical
Follow-up
5 days
Authors
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May link hyperthyroidism to AF via atrial minK remodeling; hypothesis-generating for chamber-specific channel effects in humans.
Does triiodothyronine (T3) modulate the gene expression of voltage-gated potassium channels in adult rat hearts?
p-value: p=<0.001
Thyroid hormone T3 modulates the gene expression of voltage-gated potassium channels in a chamber-specific manner, particularly up-regulating minK in the atrium, which may contribute to the frequent occurrence of atrial fibrillation in hyperthyroidism.
Aizawa et al. (2000) conducted a review in Hyperthyroidism and Atrial Fibrillation. Triiodothyronine (T3) vs. Control state was evaluated on Gene expression (mRNA) of voltage-gated potassium channels (p=<0.001). Thyroid hormone T3 up-regulated minK mRNA specifically in the rat atrium, which may contribute to the frequent occurrence of atrial fibrillation in hyperthyroidism.
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