Journal
CARDIOVASCULAR RESEARCH
Volume 108, Issue 1, Pages 21-30Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvv213
Keywords
TRPM4; Calcium-activated non-selective cation channel; Cardioprotection; Brugada; Arrhythmias
Categories
Funding
- French Ministere de l'Enseignement et de la Recherche
- Projet de Recherche Clinique
- foundation Renaud Febvre
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TRPM4 forms a non-selective cation channel activated by internal Ca2+. 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.
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