Key result
Pitx2c-knockdown in human atrial fibroblasts increased migration and calcium influx with enhanced phosphorylation of CaMKII, suggesting Pitx2c downregulation regulates atrial fibrosis.
Why the study?
Pitx2c deficiency increases AF risk, enhances profibrotic TGF-beta expression, and causes calcium dysregulation, but whether it modulates cardiac fibroblast activity remained unknown.
Does Pitx2c knockdown increase atrial fibroblast activity in human atrial fibroblasts?
Population
Human atrial fibroblasts (HAFs)
Comparison
Pitx2c-knockdown HAFs vs control HAFs
Design
In vitro controlled preclinical study
Authors
Loading...
Pitx2c modulation should not yet inform AF therapy; leaves open its mechanistic role in fibroblast activity and fibrosis.
Does Pitx2c knockdown increase atrial fibroblast activity in human atrial fibroblasts?
Downregulation of Pitx2c increases atrial fibroblast migration and calcium influx via CaMKII, suggesting a mechanism for atrial fibrosis and arrhythmogenesis in atrial fibrillation.
Kao et al. (2019) studied Atrial fibrillation and atrial fibrosis. Pitx2c-knockdown using shRNA or siRNA vs. Control human atrial fibroblasts was evaluated on Fibroblast migration, proliferation, and calcium influx. Pitx2c-knockdown in human atrial fibroblasts increased migration and calcium influx with enhanced phosphorylation of CaMKII, suggesting Pitx2c downregulation regulates atrial fibrosis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: