Key result
Cardiac myocyte-specific overexpression of ETV1 in mice induced atrial dilatation, fibrosis, and arrhythmia, whereas ETV1 ablation prevented Ang II-induced atrial remodeling.
Population
Human atrial tissue from patients with permanent atrial fibrillation; mice with cardiac myocyte-specific…
Comparison
Cardiac myocyte-specific overexpression of ETV1… vs Control mice
Design
Preclinical
Follow-up
2 weeks (for Ang II treatment)
Authors
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ETV1 inhibition merits testing in translational models; leaves open any role in human AF management.
The transcription factor ETV1 is a critical mediator of atrial structural remodeling and arrhythmia, presenting a potential novel therapeutic target for atrial fibrillation.
Rommel et al. (2018) studied Atrial fibrillation. ETV1 overexpression or ablation vs. Control mice was evaluated on Atrial remodeling, fibrosis, thrombosis, and arrhythmia. Cardiac myocyte-specific overexpression of ETV1 in mice induced atrial dilatation, fibrosis, and arrhythmia, whereas ETV1 ablation prevented Ang II-induced atrial remodeling.
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