Why the study?
Atrial structural remodeling and fibroblast differentiation drive persistent atrial fibrillation, but the underlying molecular mechanisms remain poorly understood.
Population
Atrial fibroblasts from patients with atrial fibrillation and patients with sinus rhythm
Comparison
Inhibition of CDK1, paxillin mutation, or shRNA knockdown vs controls
Design
In vitro experimental study
Authors
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May support CDK1-paxillin inhibition to limit atrial fibrosis; leaves open translation to human AF prevention.
Phosphorylation of paxillin at Ser244 by CDK1 drives atrial fibroblast differentiation, highlighting a potential molecular target to prevent atrial fibrosis in atrial fibrillation.
Chen et al. (2019) studied this question.
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