TREK-1 (K2P2.1) K+ channels are suppressed in patients with atrial fibrillation and heart failure and provide therapeutic targets for rhythm control
暂无分享,去创建一个
C. Bruehl | M. Karck | H. Katus | N. Frey | Dierk Thomas | J. Franke | P. Lugenbiel | D. Frank | T. Weis | B. Schmack | A. Ruhparwar | P. Schweizer | C. Seyler | Pascal Geschwill | Katharina Govorov | Pascal Syren | Fabian Wenz
[1] P. Kirchhof,et al. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. , 2016, European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery.
[2] P. Kirchhof,et al. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. , 2016, Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology.
[3] P. Kirchhof,et al. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. , 2016, European heart journal.
[4] H. Pak,et al. Prolonged atrial refractoriness predicts the onset of atrial fibrillation: A 12-year follow-up study. , 2016, Heart rhythm.
[5] M. Borggrefe,et al. Upregulation of K2P3.1 K+ Current Causes Action Potential Shortening in Patients With Chronic Atrial Fibrillation , 2015, Circulation.
[6] X. Wehrens,et al. Expression and function of Kv1.1 potassium channels in human atria from patients with atrial fibrillation , 2015, Basic Research in Cardiology.
[7] H. Katus,et al. Atrial Fibrillation Complicated by Heart Failure Induces Distinct Remodeling of Calcium Cycling Proteins , 2015, PloS one.
[8] Xiaobin Luo,et al. Fibroblast inward-rectifier potassium current upregulation in profibrillatory atrial remodeling. , 2015, Circulation research.
[9] H. Katus,et al. Modulation of K2P2.1 and K2P10.1 K+ channel sensitivity to carvedilol by alternative mRNA translation initiation , 2014, British journal of pharmacology.
[10] H. Katus,et al. Inhibition of cardiac two-pore-domain K+ (K2P) channels--an emerging antiarrhythmic concept. , 2014, European journal of pharmacology.
[11] A. Draguhn,et al. The symptom complex of familial sinus node dysfunction and myocardial noncompaction is associated with mutations in the HCN4 channel. , 2014, Journal of the American College of Cardiology.
[12] W. Wenzel,et al. Cardiac expression and atrial fibrillation-associated remodeling of K₂p2.1 (TREK-1) K⁺ channels in a porcine model. , 2014, Life sciences.
[13] Nazem Akoum,et al. Association of atrial tissue fibrosis identified by delayed enhancement MRI and atrial fibrillation catheter ablation: the DECAAF study. , 2014, JAMA.
[14] H. Katus,et al. Suppression of persistent atrial fibrillation by genetic knockdown of caspase 3: a pre-clinical pilot study. , 2013, European heart journal.
[15] H. Katus,et al. Biological Heart Rate Reduction Through Genetic Suppression of Gαs Protein in the Sinoatrial Node , 2012, Journal of the American Heart Association.
[16] S. Nattel,et al. Novel molecular targets for atrial fibrillation therapy , 2012, Nature Reviews Drug Discovery.
[17] H. Katus,et al. Genetic suppression of Gαs protein provides rate control in atrial fibrillation , 2012, Basic Research in Cardiology.
[18] H. Katus,et al. Genetic suppression of atrial fibrillation using a dominant-negative ether-a-go-go-related gene mutant. , 2012, Heart rhythm.
[19] M. Koch,et al. Connexin 43 gene therapy prevents persistent atrial fibrillation in a porcine model. , 2011, Cardiovascular research.
[20] James Elber Duverger,et al. Arrhythmogenic left atrial cellular electrophysiology in a murine genetic long QT syndrome model. , 2011, Cardiovascular research.
[21] Niels Voigt,et al. Recent advances in the molecular pathophysiology of atrial fibrillation. , 2011, The Journal of clinical investigation.
[22] S. Nattel,et al. Molecular determinants of cardiac fibroblast electrical function and therapeutic implications for atrial fibrillation. , 2011, Cardiovascular research.
[23] E. Isacoff,et al. Optical probing of a dynamic membrane interaction that regulates the TREK1 channel , 2011, Proceedings of the National Academy of Sciences.
[24] G. Breithardt,et al. Knock-in gain-of-function sodium channel mutation prolongs atrial action potentials and alters atrial vulnerability. , 2010, Heart rhythm.
[25] Péter Enyedi,et al. Molecular Background of Leak K (cid:1) Currents: Two-Pore Domain Potassium Channels , 2010 .
[26] G. Breithardt,et al. Atrial Arrhythmias in Long‐QT Syndrome under Daily Life Conditions: A Nested Case Control Study , 2009, Journal of cardiovascular electrophysiology.
[27] S. Nattel,et al. Atrial structural remodeling as an antiarrhythmic target. , 2008, Journal of cardiovascular pharmacology.
[28] Dierk Thomas,et al. Alternative Translation Initiation in Rat Brain Yields K2P2.1 Potassium Channels Permeable to Sodium , 2008, Neuron.
[29] Stanley Nattel,et al. Calcium-Handling Abnormalities Underlying Atrial Arrhythmogenesis and Contractile Dysfunction in Dogs With Congestive Heart Failure , 2008, Circulation. Arrhythmia and electrophysiology.
[30] S. Nattel,et al. Arrhythmogenic ion-channel remodeling in the heart: heart failure, myocardial infarction, and atrial fibrillation. , 2007, Physiological reviews.
[31] Stanley Nattel,et al. Atrial Ionic Remodeling Induced by Atrial Tachycardia in the Presence of Congestive Heart Failure , 2004, Circulation.
[32] J. K. Donahue,et al. Pathophysiological findings in a model of persistent atrial fibrillation and severe congestive heart failure. , 2004, Cardiovascular research.
[33] S. Nattel,et al. Evolution of the atrial fibrillation substrate in experimental congestive heart failure: angiotensin-dependent and -independent pathways. , 2003, Cardiovascular research.
[34] G. Breithardt,et al. Prolonged Atrial Action Potential Durations and Polymorphic Atrial Tachyarrhythmias in Patients with Long QT Syndrome , 2003, Journal of cardiovascular electrophysiology.
[35] S. Nattel,et al. Consequences of Atrial Tachycardia-Induced Remodeling Depend on the Preexisting Atrial Substrate , 2002, Circulation.
[36] Detlef Bockenhauer,et al. Potassium leak channels and the KCNK family of two-p-domain subunits , 2001, Nature Reviews Neuroscience.
[37] G. Breithardt,et al. A Patient with “Atrial Torsades de Pointes” , 2000, Journal of cardiovascular electrophysiology.
[38] John Calvin Reed,et al. Myocardial cell death in fibrillating and dilated human right atria. , 1999, Journal of the American College of Cardiology.
[39] M. Borggrefe,et al. Upregulation of K 2 P 3 . 1 K + Current Causes Action Potential Shortening in Patients With Chronic Atrial Fibrillation , 2015 .
[40] P. Kirchhof,et al. Pathophysiological mechanisms of atrial fibrillation: a translational appraisal. , 2011, Physiological reviews.
[41] S. Nattel,et al. Atrial Fibrillation Atrial Fibrillation Pathophysiology Implications for Management , 2011 .