Upregulation of K(2P)3.1 K+ Current Causes Action Potential Shortening in Patients With Chronic Atrial Fibrillation.

@article{Schmidt2015UpregulationOK,
  title={Upregulation of K(2P)3.1 K+ Current Causes Action Potential Shortening in Patients With Chronic Atrial Fibrillation.},
  author={Constanze Schmidt and Felix Wiedmann and Niels Voigt and Xiao-Bo Zhou and Jordi Heijman and Siegfried Lang and Virginia Albert and Stefan M. Kallenberger and Arjang Ruhparwar and G{\'a}bor Szab{\'o} and Klaus Kallenbach and Matthias Karck and Martin Borggrefe and P{\'e}ter Biliczki and Joachim R. Ehrlich and Istv{\'a}n Baczk{\'o} and Patrick Lugenbiel and Patrick Schweizer and Birgit C. Donner and Hugo A. Katus and Dobromir Dobrev and Dierk Thomas},
  journal={Circulation},
  year={2015},
  volume={132 2},
  pages={82-92}
}
BACKGROUND Antiarrhythmic management of atrial fibrillation (AF) remains a major clinical challenge. Mechanism-based approaches to AF therapy are sought to increase effectiveness and to provide individualized patient care. K(2P)3.1 (TASK-1 [tandem of P domains in a weak inward-rectifying K+ channel-related acid-sensitive K+ channel-1]) 2-pore-domain K+ (K(2P)) channels have been implicated in action potential regulation in animal models. However, their role in the pathophysiology and treatment… CONTINUE READING
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