HDAC2-dependent remodeling of KCa2.2 (KCNN2) and KCa2.3 (KCNN3) K+ channels in atrial fibrillation with concomitant heart failure-Reference-Cited by-同舟云学术

HDAC2-dependent remodeling of KCa2.2 (KCNN2) and KCa2.3 (KCNN3) K+ channels in atrial fibrillation with concomitant heart failure

Published:2021-02 Issue: Volume:266 Page:118892
ISSN:0024-3205
Container-title:Life Sciences
language:en
Short-container-title:Life Sciences

Author:

Rahm Ann-Kathrin,Wieder Teresa,Gramlich Dominik,Müller Mara Elena,Wunsch Maximilian N.,El Tahry Fadwa A.,Heimberger Tanja,Weis Tanja,Most Patrick,Katus Hugo A.,Thomas Dierk,Lugenbiel Patrick

Funder

University of Heidelberg

German Cardiac Society

Elisabeth und Rudolf-Hirsch Stiftung für Medizinische Forschung

Ernst und Berta Grimmke-Stiftung

German Heart Foundation

German Internal Medicine Society

Deutsche Forschungsgemeinschaft

Ministry of Science, Research and the Arts Baden-Wuerttemberg

Cardiology Career Program of the Department of Cardiology

Publisher

Elsevier BV

Subject

General Pharmacology, Toxicology and Pharmaceutics,General Biochemistry, Genetics and Molecular Biology,General Medicine

Reference36 articles.

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2. TREK-1 (K2P2.1) K+ channels are suppressed in patients with atrial fibrillation and heart failure and provide therapeutic targets for rhythm control;Lugenbiel;Basic Res. Cardiol.,2017

3. Schmidt C, Wiedmann F, Zhou XB, et al. Inverse remodeling of K2P3.1 K+ channel expression and action potential duration in left ventricular dysfunction and atrial fibrillation: implications for patient-specific antiarrhythmic drug therapy. Eur. Heart J. 2017;38:1764–1774.

4. Prolonged atrial refractoriness predicts the onset of atrial fibrillation: a 12-year follow-up study;Lee;Heart Rhythm.,2016

5. Small-conductance Ca2+-activated K+ channels and cardiac arrhythmias;Zhang;Heart Rhythm.,2015

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