Physiological roles of the transient outward current Ito in normal and diseased hearts

Research output: Contribution to journalJournal articleResearchpeer-review

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Physiological roles of the transient outward current Ito in normal and diseased hearts. / Cordeiro, Jonathan M.; Callø, Kirstine; Aschar-Sobbi, Roozbeh; Kim, Kyoung-Han; Korogyi, Adam; Occhipinti, Dona; Backx, Peter H.; Panama, Brian K.

In: Frontiers in bioscience (Scholar edition), Vol. 8, 454, 01.01.2016, p. 143-159.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Cordeiro, JM, Callø, K, Aschar-Sobbi, R, Kim, K-H, Korogyi, A, Occhipinti, D, Backx, PH & Panama, BK 2016, 'Physiological roles of the transient outward current Ito in normal and diseased hearts', Frontiers in bioscience (Scholar edition), vol. 8, 454, pp. 143-159. https://doi.org/10.2741/S454

APA

Cordeiro, J. M., Callø, K., Aschar-Sobbi, R., Kim, K-H., Korogyi, A., Occhipinti, D., Backx, P. H., & Panama, B. K. (2016). Physiological roles of the transient outward current Ito in normal and diseased hearts. Frontiers in bioscience (Scholar edition), 8, 143-159. [454]. https://doi.org/10.2741/S454

Vancouver

Cordeiro JM, Callø K, Aschar-Sobbi R, Kim K-H, Korogyi A, Occhipinti D et al. Physiological roles of the transient outward current Ito in normal and diseased hearts. Frontiers in bioscience (Scholar edition). 2016 Jan 1;8:143-159. 454. https://doi.org/10.2741/S454

Author

Cordeiro, Jonathan M. ; Callø, Kirstine ; Aschar-Sobbi, Roozbeh ; Kim, Kyoung-Han ; Korogyi, Adam ; Occhipinti, Dona ; Backx, Peter H. ; Panama, Brian K. / Physiological roles of the transient outward current Ito in normal and diseased hearts. In: Frontiers in bioscience (Scholar edition). 2016 ; Vol. 8. pp. 143-159.

Bibtex

@article{56797b95c87148529830847a5ea875e6,
title = "Physiological roles of the transient outward current Ito in normal and diseased hearts",
abstract = "The Ca2+-independent transient outward K+ current (Ito) plays a critical role in underlying phase 1 of repolarization of the cardiac action potential and, as a result, is central to modulating excitation-contraction coupling and propensity for arrhythmia. Additionally, Ito and its molecular constituents are consistently reduced in cardiac hypertrophy and heart failure. In this review, we discuss the physiological role of Ito as well as the molecular basis of this current in human and canine hearts, in which Ito has been thoroughly studied. In particular, we discuss the role of Ito in the action potential and the mechanisms by which Ito modulates excitation-contraction coupling. We also describe the effects of mutations in the subunits constituting the Ito channel as well as the role of Ito in the failing myocardium. Finally, we review pharmacological modulation of Ito and discuss the evidence supporting the hypothesis that restoration of Ito in the setting of heart failure may be therapeutically beneficial by enhancing excitation-contraction coupling and cardiac function.",
author = "Cordeiro, {Jonathan M.} and Kirstine Call{\o} and Roozbeh Aschar-Sobbi and Kyoung-Han Kim and Adam Korogyi and Dona Occhipinti and Backx, {Peter H.} and Panama, {Brian K.}",
year = "2016",
month = jan,
day = "1",
doi = "10.2741/S454",
language = "English",
volume = "8",
pages = "143--159",
journal = "Frontiers in Bioscience - Scholar",
issn = "1945-0516",
publisher = "Frontiers in Bioscience",

}

RIS

TY - JOUR

T1 - Physiological roles of the transient outward current Ito in normal and diseased hearts

AU - Cordeiro, Jonathan M.

AU - Callø, Kirstine

AU - Aschar-Sobbi, Roozbeh

AU - Kim, Kyoung-Han

AU - Korogyi, Adam

AU - Occhipinti, Dona

AU - Backx, Peter H.

AU - Panama, Brian K.

PY - 2016/1/1

Y1 - 2016/1/1

N2 - The Ca2+-independent transient outward K+ current (Ito) plays a critical role in underlying phase 1 of repolarization of the cardiac action potential and, as a result, is central to modulating excitation-contraction coupling and propensity for arrhythmia. Additionally, Ito and its molecular constituents are consistently reduced in cardiac hypertrophy and heart failure. In this review, we discuss the physiological role of Ito as well as the molecular basis of this current in human and canine hearts, in which Ito has been thoroughly studied. In particular, we discuss the role of Ito in the action potential and the mechanisms by which Ito modulates excitation-contraction coupling. We also describe the effects of mutations in the subunits constituting the Ito channel as well as the role of Ito in the failing myocardium. Finally, we review pharmacological modulation of Ito and discuss the evidence supporting the hypothesis that restoration of Ito in the setting of heart failure may be therapeutically beneficial by enhancing excitation-contraction coupling and cardiac function.

AB - The Ca2+-independent transient outward K+ current (Ito) plays a critical role in underlying phase 1 of repolarization of the cardiac action potential and, as a result, is central to modulating excitation-contraction coupling and propensity for arrhythmia. Additionally, Ito and its molecular constituents are consistently reduced in cardiac hypertrophy and heart failure. In this review, we discuss the physiological role of Ito as well as the molecular basis of this current in human and canine hearts, in which Ito has been thoroughly studied. In particular, we discuss the role of Ito in the action potential and the mechanisms by which Ito modulates excitation-contraction coupling. We also describe the effects of mutations in the subunits constituting the Ito channel as well as the role of Ito in the failing myocardium. Finally, we review pharmacological modulation of Ito and discuss the evidence supporting the hypothesis that restoration of Ito in the setting of heart failure may be therapeutically beneficial by enhancing excitation-contraction coupling and cardiac function.

U2 - 10.2741/S454

DO - 10.2741/S454

M3 - Journal article

C2 - 26709904

VL - 8

SP - 143

EP - 159

JO - Frontiers in Bioscience - Scholar

JF - Frontiers in Bioscience - Scholar

SN - 1945-0516

M1 - 454

ER -

ID: 154794359