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TREK-1 in the heart: Potential physiological and pathophysiological roles
Frontiers in physiology, 2022, Vol.13
[Peer Reviewed Journal]
Distributed under a Creative Commons Attribution 4.0 International License ;ISSN: 1664-042X ;EISSN: 1664-042X ;DOI: 10.3389/fphys.2022.1095102
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Title:
TREK-1 in the heart: Potential physiological and pathophysiological roles
Author:
Bechard, Emilie
;
Bride, Jamie
;
Le Guennec, Jean-Yves
;
Brette, Fabien
;
Demion, Marie
Subjects:
Cardiology and cardiovascular system
;
Human health and pathology
;
Life Sciences
;
Tissues and Organs
Is Part Of:
Frontiers in physiology, 2022, Vol.13
Description:
The TREK-1 channel belongs to the TREK subfamily of two-pore domains channels that are activated by stretch and polyunsaturated fatty acids and inactivated by Protein Kinase A phosphorylation. The activation of this potassium channel must induce a hyperpolarization of the resting membrane potential and a shortening of the action potential duration in neurons and cardiac cells, two phenomena being beneficial for these tissues in pathological situations like ischemia-reperfusion. Surprisingly, the physiological role of TREK-1 in cardiac function has never been thoroughly investigated, very likely because of the lack of a specific inhibitor. However, possible roles have been unraveled in pathological situations such as atrial fibrillation worsened by heart failure, right ventricular outflow tract tachycardia or pulmonary arterial hypertension. The inhomogeneous distribution of TREK-1 channel within the heart reinforces the idea that this stretch-activated potassium channel might play a role in cardiac areas where the mechanical constraints are important and need a particular protection afforded by TREK-1. Consequently, the main purpose of this mini review is to discuss the possible role played by TREK -1 in physiological and pathophysiological conditions and its potential role in mechano-electrical feedback. Improved understanding of the role of TREK-1 in the heart may help the development of promising treatments for challenging cardiac diseases.
Publisher:
Frontiers
Language:
English
Identifier:
ISSN: 1664-042X
EISSN: 1664-042X
DOI: 10.3389/fphys.2022.1095102
Source:
Hyper Article en Ligne (HAL) (Open Access)
GFMER Free Medical Journals
NCBI PubMed Central(免费)
ROAD: Directory of Open Access Scholarly Resources
DOAJ Directory of Open Access Journals
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