This week, two new papers that were recently accepted have become available online. In the first paper, a collaboration with the group of Prof. Dierk Thomas, Heidelberg University, we investigated the role K2P3.1 channel remodeling in patients with atrial fibrillation and/or left ventricular dysfunction. We found opposite regulation of these channels in both conditions, which affects the channel’s potential as an antiarrhythmic target and highlights the need for tailored therapeutic approaches. In the second paper, we review the role of serine/threonine phosphatases in atrial fibrillation.
Serine/Threonine Phosphatases in Atrial Fibrillation.
Heijman J, Ghezelbash S, Wehrens XH, Dobrev D.
J Mol Cell Cardiol. 2017 Jan 7. Epub ahead of print [Pubmed]
Inverse remodelling of K2P3.1 K+ channel expression and action potential duration in left ventricular dysfunction and atrial fibrillation: implications for patient-specific antiarrhythmic drug therapy.
Schmidt C, Wiedmann F, Zhou XB, Heijman J, Voigt N, Ratte A, Lang S, Kallenberger SM, Campana C, Weymann A, De Simone R, Szabo G, Ruhparwar A, Kallenbach K, Karck M, Ehrlich JR, Baczkó I, Borggrefe M, Ravens U, Dobrev D, Katus HA, Thomas D.
Eur Heart J. 2017 Jan 4. Epub ahead of print [Pubmed]