Abstract
K(+) channels are fundamental determinants of cardiac repolarization, with distinct channel families shaping atrial and ventricular electrophysiology. Dysregulation of these channels underlies both inherited and acquired cardiac arrhythmias, making them central to therapeutic development. Recent advances, ranging from structural studies to translational and clinical investigations, underscore K(+) channels as critical therapeutic targets. In particular, recent studies on small conductance Ca(2+)-activated K(+) (SK or K(Ca)2), TASK-1, and KCNQ1 channels have offered new insights from atrial-selective drug designs to precision antiarrhythmic strategies, respectively.