TY - JOUR
T1 - Potassium channels in the heart
T2 - structure, function and regulation
AU - Grandi, Eleonora
AU - Sanguinetti, Michael C.
AU - Bartos, Daniel C.
AU - Bers, Donald M.
AU - Chen-Izu, Ye
AU - Chiamvimonvat, Nipavan
AU - Colecraft, Henry M.
AU - Delisle, Brian P.
AU - Heijman, Jordi
AU - Navedo, Manuel F.
AU - Noskov, Sergei
AU - Proenza, Catherine
AU - Vandenberg, Jamie I.
AU - Yarov-Yarovoy, Vladimir
N1 - Publisher Copyright:
© 2016 The Authors. The Journal of Physiology © 2016 The Physiological Society
PY - 2017/4/1
Y1 - 2017/4/1
N2 - Abstract: This paper is the outcome of the fourth UC Davis Systems Approach to Understanding Cardiac Excitation–Contraction Coupling and Arrhythmias Symposium, a biannual event that aims to bring together leading experts in subfields of cardiovascular biomedicine to focus on topics of importance to the field. The theme of the 2016 symposium was ‘K+ Channels and Regulation’. Experts in the field contributed their experimental and mathematical modelling perspectives and discussed emerging questions, controversies and challenges on the topic of cardiac K+ channels. This paper summarizes the topics of formal presentations and informal discussions from the symposium on the structural basis of voltage-gated K+ channel function, as well as the mechanisms involved in regulation of K+ channel gating, expression and membrane localization. Given the critical role for K+ channels in determining the rate of cardiac repolarization, it is hardly surprising that essentially every aspect of K+ channel function is exquisitely regulated in cardiac myocytes. This regulation is complex and highly interrelated to other aspects of myocardial function. K+ channel regulatory mechanisms alter, and are altered by, physiological challenges, pathophysiological conditions, and pharmacological agents. An accompanying paper focuses on the integrative role of K+ channels in cardiac electrophysiology, i.e. how K+ currents shape the cardiac action potential, and how their dysfunction can lead to arrhythmias, and discusses K+ channel-based therapeutics. A fundamental understanding of K+ channel regulatory mechanisms and disease processes is fundamental to reveal new targets for human therapy.
AB - Abstract: This paper is the outcome of the fourth UC Davis Systems Approach to Understanding Cardiac Excitation–Contraction Coupling and Arrhythmias Symposium, a biannual event that aims to bring together leading experts in subfields of cardiovascular biomedicine to focus on topics of importance to the field. The theme of the 2016 symposium was ‘K+ Channels and Regulation’. Experts in the field contributed their experimental and mathematical modelling perspectives and discussed emerging questions, controversies and challenges on the topic of cardiac K+ channels. This paper summarizes the topics of formal presentations and informal discussions from the symposium on the structural basis of voltage-gated K+ channel function, as well as the mechanisms involved in regulation of K+ channel gating, expression and membrane localization. Given the critical role for K+ channels in determining the rate of cardiac repolarization, it is hardly surprising that essentially every aspect of K+ channel function is exquisitely regulated in cardiac myocytes. This regulation is complex and highly interrelated to other aspects of myocardial function. K+ channel regulatory mechanisms alter, and are altered by, physiological challenges, pathophysiological conditions, and pharmacological agents. An accompanying paper focuses on the integrative role of K+ channels in cardiac electrophysiology, i.e. how K+ currents shape the cardiac action potential, and how their dysfunction can lead to arrhythmias, and discusses K+ channel-based therapeutics. A fundamental understanding of K+ channel regulatory mechanisms and disease processes is fundamental to reveal new targets for human therapy.
KW - gating
KW - heterogeneity
KW - phosphorylation
KW - trafficking
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U2 - 10.1113/JP272864
DO - 10.1113/JP272864
M3 - Article
C2 - 27861921
AN - SCOPUS:85006000170
SN - 0022-3751
VL - 595
SP - 2209
EP - 2228
JO - Journal of Physiology
JF - Journal of Physiology
IS - 7
ER -