Why the study?
Rapid electrical stimulation of atrial fibroblasts plays a crucial role in AF pathogenesis, but the underlying molecular mechanisms remain unclear.
Population
Human cardiac fibroblasts from adult atria (HCF-aa)
Comparison
Rapid electrical stimulation, MALAT1 siRNA, miR-499a-5p mimics/inhibitors, and SOX6 overexpression
Design
In vitro controlled laboratory study
Key result
In human cardiac fibroblasts under rapid electrical stimulation, increased exosomal MALAT1 expression peaked at 2 hours and counteracted miR-499-5p's suppression of SOX6.
Authors
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Offers candidate AF pathway for cell-free targeting; leaves open in vivo validation before any clinical consideration.
In human atrial fibroblasts, rapid electrical stimulation induces exosomal MALAT1, which upregulates SOX6 by sponging miR-499a-5p, highlighting a potential molecular pathway and cell-free therapeutic target in atrial fibrillation pathogenesis.
Chuang et al. (2024) studied Atrial fibrillation. Rapid electrical stimulation (RES) was evaluated on Expression levels of MALAT1, miR-499a-5p, and SOX6. In human cardiac fibroblasts under rapid electrical stimulation, increased exosomal MALAT1 expression peaked at 2 hours and counteracted miR-499-5p's suppression of SOX6.