TREK-1 in the heart: Potential physiological and pathophysiological roles

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...

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Main Authors: Emilie Bechard, Jamie Bride, Jean-Yves Le Guennec, Fabien Brette, Marie Demion
Format: Article
Language:English
Published: Frontiers Media S.A. 2022-12-01
Series:Frontiers in Physiology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fphys.2022.1095102/full
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author Emilie Bechard
Jamie Bride
Jean-Yves Le Guennec
Fabien Brette
Marie Demion
author_facet Emilie Bechard
Jamie Bride
Jean-Yves Le Guennec
Fabien Brette
Marie Demion
author_sort Emilie Bechard
collection DOAJ
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.
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spelling doaj.art-b798a5deea3047249dd678bb716180e72022-12-22T15:56:27ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2022-12-011310.3389/fphys.2022.10951021095102TREK-1 in the heart: Potential physiological and pathophysiological rolesEmilie BechardJamie BrideJean-Yves Le GuennecFabien BretteMarie DemionThe 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.https://www.frontiersin.org/articles/10.3389/fphys.2022.1095102/fullTREK-1K2P2.1atrial fibrillationmyocardial infarctionRVOT
spellingShingle Emilie Bechard
Jamie Bride
Jean-Yves Le Guennec
Fabien Brette
Marie Demion
TREK-1 in the heart: Potential physiological and pathophysiological roles
Frontiers in Physiology
TREK-1
K2P2.1
atrial fibrillation
myocardial infarction
RVOT
title TREK-1 in the heart: Potential physiological and pathophysiological roles
title_full TREK-1 in the heart: Potential physiological and pathophysiological roles
title_fullStr TREK-1 in the heart: Potential physiological and pathophysiological roles
title_full_unstemmed TREK-1 in the heart: Potential physiological and pathophysiological roles
title_short TREK-1 in the heart: Potential physiological and pathophysiological roles
title_sort trek 1 in the heart potential physiological and pathophysiological roles
topic TREK-1
K2P2.1
atrial fibrillation
myocardial infarction
RVOT
url https://www.frontiersin.org/articles/10.3389/fphys.2022.1095102/full
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