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Cardiovasc Res. 2015 Oct 1;108(1):21-30. doi: 10.1093/cvr/cvv213. Epub 2015 Aug 13.

TRPM4 in cardiac electrical activity.

Author information

1
Groupe Signalisation, Electrophysiologie et Imagerie des Lésions d'Ischémie-Reperfusion Myocardique, EA4650, Université de Caen Basse-Normandie, Sciences D, Esplanade de la Paix, CS 14032, 14032 Caen Cedex 5, France romain.guinamard@unicaen.fr.
2
EA 4173, Université Lyon 1 and Hôpital du Nord-Ouest, Lyon, France.
3
Groupe Signalisation, Electrophysiologie et Imagerie des Lésions d'Ischémie-Reperfusion Myocardique, EA4650, Université de Caen Basse-Normandie, Sciences D, Esplanade de la Paix, CS 14032, 14032 Caen Cedex 5, France.
4
Department of Anatomy, Hainan Medical College, Haikou, Hainan 571101, China.

Abstract

TRPM4 forms a non-selective cation channel activated by internal Ca(2+). Its functional expression was demonstrated in cardiomyocytes of several mammalian species including humans, but the channel is also present in many other tissues. The recent characterization of the TRPM4 inhibitor 9-phenanthrol, and the availability of transgenic mice have helped to clarify the role of TRPM4 in cardiac electrical activity, including diastolic depolarization from the sino-atrial node cells in mouse, rat, and rabbit, as well as action potential duration in mouse cardiomyocytes. In rat and mouse, pharmacological inhibition of TRPM4 prevents cardiac ischaemia-reperfusion injuries and decreases the occurrence of arrhythmias. Several studies have identified TRPM4 mutations in patients with inherited cardiac diseases including conduction blocks and Brugada syndrome. This review identifies TRPM4 as a significant actor in cardiac electrophysiology.

KEYWORDS:

Arrhythmias; Brugada; Calcium-activated non-selective cation channel; Cardioprotection; TRPM4

PMID:
26272755
DOI:
10.1093/cvr/cvv213
[Indexed for MEDLINE]

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