Publications by authors named "Maximilian N Wunsch"
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.
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- Atrial fibrillation (AF) combined with heart failure (HF) leads to longer atrial refractoriness and is linked to reduced expression of small-conductance calcium-activated K channels (KCNN2 and KCNN3), as well as downregulation of histone deacetylase 2 (HDAC2).
- Research involved measuring transcript levels of HDAC2 and KCNN2/3 in both AF/HF patients and a pig model, along with experiments in atrial myocytes to observe the effects of HDAC2 inactivation.
- Findings suggest that increased heart rates may trigger epigenetic changes affecting KCNN expression, indicating potential targets for further research on therapeutic approaches in the context of AF with heart failure.