Atrial fibrillation and heart failure-associated remodeling of two-pore-domain potassium (K) channels in murine disease models: focus on TASK-1.

Understanding molecular mechanisms involved in atrial tissue remodeling and arrhythmogenesis in atrial fibrillation (AF) is essential for developing specific therapeutic approaches. Two-pore-domain potassium (K) channels modulate cellular excitability, and TASK-1 (K3.1) currents were recently shown to alter atrial action potential duration in AF and heart failure (HF).

Adrenergic Stress Protection of Human iPS Cell-Derived Cardiomyocytes by Fast K7.1 Recycling.

The fight-or-flight response (FFR), a physiological acute stress reaction, involves positive chronotropic and inotropic effects on heart muscle cells mediated through β-adrenoceptor activation. Increased systolic calcium is required to enable stronger heart contractions whereas elevated potassium currents are to limit the duration of the action potentials and prevent arrhythmia. The latter effect is accomplished by an increased functional activity of the K7.