Why the study?
Pathogenic TRPM4 variants are linked to inherited cardiac diseases, but the cardiac electrophysiological phenotypes in Trpm4 knockdown mouse models remain incompletely characterized.
Population
Isolated atrial and ventricular cardiac myocytes and explanted or in vivo mouse hearts
Comparison
Trpm4 deletion vs control
Design
Preclinical laboratory and electrophysiological study
Key result
Deletion of Trpm4 in murine cardiac myocytes reduced peak Na+ currents, increased sensitivity to mexiletine, and slowed intraventricular conduction.
Authors
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TRPM4 variants merit inclusion in arrhythmia genetic panels; leaves open therapeutic targeting of channel trafficking.
TRPM4 expression regulates Nav1.5 function in murine cardiac myocytes, with its deletion reducing peak Na+ currents and slowing intraventricular conduction.
Ozhathil et al. (2021) studied Trpm4 deletion. Trpm4 deletion was evaluated on Peak Na+ currents and intraventricular conduction. Deletion of Trpm4 in murine cardiac myocytes reduced peak Na+ currents, increased sensitivity to mexiletine, and slowed intraventricular conduction.
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