Key result
Late INa enhancement increases SR-Ca2+-leak in atrial myocardium via CaMKII and PKA activation, and late INa inhibition attenuates this leak in murine and human atrial fibrillation models.
Population
Murine atrial cardiomyocytes and atrial cardiomyocytes from patients with atrial fibrillation
Comparison
Late INa enhancement with Anemonia sulcata toxin… vs Unstimulated cells or cells without specific…
Design
Preclinical
Authors
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Hypothesis-generating for CaMKII as late INa-SR Ca leak intermediary in atria; leaves open clinical translation to human AF.
Late INa increases diastolic SR-Ca2+-leak in atrial myocardium via CaMKII and PKA activation, suggesting late INa inhibition as a potential antiarrhythmic strategy in atrial fibrillation.
Fischer et al. (2015) studied Atrial fibrillation. Late INa inhibition was evaluated on SR-Ca2+-leak. Late INa enhancement increases SR-Ca2+-leak in atrial myocardium via CaMKII and PKA activation, and late INa inhibition attenuates this leak in murine and human atrial fibrillation models.
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