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...
Gespeichert in:
| Hauptverfasser: | , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
2021
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| In: |
Progress in biophysics & molecular biology
Year: 2020, Jahrgang: 159, Pages: 126-135 |
| ISSN: | 1873-1732 |
| DOI: | 10.1016/j.pbiomolbio.2020.05.007 |
| Online-Zugang: | 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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| Verfasserangaben: | Felix Wiedmann, Susanne Rinné, Birgit Donner, Niels Decher, Hugo A. Katus, Constanze Schmidt |
MARC
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| 245 | 1 | 0 | |a Mechanosensitive TREK-1 two-pore-domain potassium (K2P) channels in the cardiovascular system |c Felix Wiedmann, Susanne Rinné, Birgit Donner, Niels Decher, Hugo A. Katus, Constanze Schmidt |
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| 520 | |a 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. | ||
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| 650 | 4 | |a Arrhythmia | |
| 650 | 4 | |a K2.1 | |
| 650 | 4 | |a Mechanoelectrical feedback | |
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| 650 | 4 | |a TREK-1 | |
| 700 | 1 | |a Rinné, Susanne |e VerfasserIn |4 aut | |
| 700 | 1 | |a Donner, Birgit |e VerfasserIn |4 aut | |
| 700 | 1 | |a Decher, Niels |e VerfasserIn |4 aut | |
| 700 | 1 | |a Katus, Hugo |d 1951- |e VerfasserIn |0 (DE-588)108916618 |0 (DE-627)577155040 |0 (DE-576)289625076 |4 aut | |
| 700 | 1 | |a Schmidt, Constanze |e VerfasserIn |0 (DE-588)1055852174 |0 (DE-627)792733142 |0 (DE-576)411903721 |4 aut | |
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