Transferrin receptor knockdown attenuates atrial fibrillation by inhibiting cardiomyocyte ferroptosis and atrial fibrosis.

Summary: Atrial fibrillation (AF) is a common heart rhythm disorder often driven by scarring (fibrosis) in the heart’s upper chambers. This study identifies a specific protein, the Transferrin receptor (TFRC), as a key culprit. TFRC allows iron to enter heart cells; when overactive, it causes a specific type of cell death called "ferroptosis" and promotes scarring. Researchers found that blocking TFRC or boosting a protective protein called FOXO3 prevented this cell death and reduced heart scarring in mice. This suggests that targeting iron uptake in heart cells could be a promising new way to treat or prevent AF.