Differential regulation of K 2.1 (KCNN1) K channel expression by histone deacetylases in atrial fibrillation with concomitant heart failure.

Atrial fibrillation (AF) with concomitant heart failure (HF) poses a significant therapeutic challenge. Mechanism-based approaches may optimize AF therapy. Small-conductance, calcium-activated K (K , KCNN) channels contribute to cardiac action potential repolarization.

Trigger-Specific Remodeling of K2 Potassium Channels in Models of Atrial Fibrillation.

Aim: Effective antiarrhythmic treatment of atrial fibrillation (AF) constitutes a major challenge, in particular, when concomitant heart failure (HF) is present. HF-associated atrial arrhythmogenesis is distinctly characterized by prolonged atrial refractoriness. Small-conductance, calcium-activated K (K, SK, ) channels contribute to cardiac action potential repolarization and are implicated in AF susceptibility and therapy.

Epigenetic regulation of cardiac electrophysiology in atrial fibrillation: HDAC2 determines action potential duration and suppresses NRSF in cardiomyocytes.

Atrial fibrillation (AF) is associated with electrical remodeling, leading to cellular electrophysiological dysfunction and arrhythmia perpetuation. Emerging evidence suggests a key role for epigenetic mechanisms in the regulation of ion channel expression. Histone deacetylases (HDACs) control gene expression through deacetylation of histone proteins.

Inhibition of cardiac K4.3 (I) channel isoforms by class I antiarrhythmic drugs lidocaine and mexiletine.

Transient outward K current, I, contributes to cardiac action potential generation and is primarily carried by K4.3 (KCND3) channels. Two K4.