Key result
Cardiomyocyte-restricted overexpression of FKBP12 in mice led to spontaneous atrial fibrillation in 57.1% (4 of 7) of transgenic mice compared to 0% (0 of 8) of controls.
Why the study?
Cardiomyocyte-restricted overexpression of FKBP12 causes spontaneous AF in mice, but the underlying mechanisms remain to be explored.
Does cardiomyocyte-restricted overexpression of FKBP12 alter atrial electrophysiology and promote spontaneous atrial fibrillation in mice?
Population
αMyHC-FKBP12 transgenic mice and nontransgenic littermate controls
Comparison
αMyHC-FKBP12 mice vs nontransgenic littermate controls
Design
Preclinical in vivo and in vitro mechanistic electrophysiology study
Authors
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Implicates cardiomyocyte FKBP12 in spontaneous AF in mice; leaves open translational relevance to human arrhythmia mechanisms.
Does cardiomyocyte-restricted overexpression of FKBP12 alter atrial electrophysiology and promote spontaneous atrial fibrillation in mice?
Absolute Event Rate: 57.1% vs 0%
Cardiomyocyte-restricted overexpression of FKBP12 in mice promotes spontaneous atrial fibrillation by reducing Nav1.5 expression and sodium current, while increasing L-type calcium current and interstitial fibrosis.
Pan et al. (2018) studied Atrial fibrillation (n=15). Cardiomyocyte-restricted overexpression of FKBP12 vs. Nontransgenic (NTG) controls was evaluated on Spontaneous atrial fibrillation. Cardiomyocyte-restricted overexpression of FKBP12 in mice led to spontaneous atrial fibrillation in 57.1% (4 of 7) of transgenic mice compared to 0% (0 of 8) of controls.
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