The mechanistic investigation remains incomplete, as we did not fully characterize upstream receptors (e.g., CXCR1/CXCR2) mediating CXCL1-induced ERS or downstream effects of TXNDC5 on cardiomyocyte apoptosis/fibrosis, nor did we explore interactions with other AF-related pathways or evaluate in vivo drug interventions targeting this axis. Here, CXCR2 is linked to atrial fibrillation.