Mechanosensitive TREK-1 two-pore-domain potassium (K2P) channels in the cardiovascular system

TWIK-related K+ channel (TREK-1) two-pore-domain potassium (K2P) channels mediate background potassium currents and regulate cellular excitability in many different types of cells. Their functional activity is controlled by a broad variety of different physiological stimuli, such as temperature, ext...

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Main Authors: Wiedmann, Felix Tobias (Author) , Rinné, Susanne (Author) , Donner, Birgit (Author) , Decher, Niels (Author) , Katus, Hugo (Author) , Schmidt, Constanze (Author)
Format: Article (Journal)
Language:English
Published: 2021
In: Progress in biophysics & molecular biology
Year: 2020, Volume: 159, Pages: 126-135
ISSN:1873-1732
DOI:10.1016/j.pbiomolbio.2020.05.007
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.pbiomolbio.2020.05.007
Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0079610720300432
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Author Notes:Felix Wiedmann, Susanne Rinné, Birgit Donner, Niels Decher, Hugo A. Katus, Constanze Schmidt
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Summary:TWIK-related K+ channel (TREK-1) two-pore-domain potassium (K2P) channels mediate background potassium currents and regulate cellular excitability in many different types of cells. Their functional activity is controlled by a broad variety of different physiological stimuli, such as temperature, extracellular or intracellular pH, lipids and mechanical stress. By linking cellular excitability to mechanical stress, TREK-1 currents might be important to mediate parts of the mechanoelectrical feedback described in the heart. Furthermore, TREK-1 currents might contribute to the dysregulation of excitability in the heart in pathophysiological situations, such as those caused by abnormal stretch or ischaemia-associated cell swelling, thereby contributing to arrhythmogenesis. In this review, we focus on the functional role of TREK-1 in the heart and its putative contribution to cardiac mechanoelectrical coupling. Its cardiac expression among different species is discussed, alongside with functional evidence for TREK-1 currents in cardiomyocytes. In addition, evidence for the involvement of TREK-1 currents in different cardiac arrhythmias, such as atrial fibrillation or ventricular tachycardia, is summarized. Furthermore, the role of TREK-1 and its interaction partners in the regulation of the cardiac heart rate is reviewed. Finally, we focus on the significance of TREK-1 in the development of cardiac hypertrophy, cardiac fibrosis and heart failure.
Item Description:Im Titel ist 2P tiefgestellt
Available online 15 June 2020
Gesehen am 05.03.2021
Physical Description:Online Resource
ISSN:1873-1732
DOI:10.1016/j.pbiomolbio.2020.05.007