Atrial APD prolongation caused by the upregulation of RAGE and subsequent INaL increase in diabetic patients

• First direct evidence that atrial APD is prolonged in diabetic patients, contrasting with the typical shortening seen in AF. • Upregulation of RAGE in diabetic atria drives an increase in late sodium current (INaL), leading to APD prolongation. • Knockdown of RAGE reduces INaL and shortens APD, suggesting a potential therapeutic target for diabetic atrial arrhythmias. • Findings highlight a novel mechanism of atrial electrical remodeling in diabetes, distinct from that in non-diabetic AF.