Nav 1.5 mutations linked to dilated cardiomyopathy phenotypes: Is the gating pore current the missing link?

Pascal Gosselin-Badaroudine; Adrien Moreau; Mohamed Chahine

doi:10.4161/chan.27179

Nav 1.5 mutations linked to dilated cardiomyopathy phenotypes: Is the gating pore current the missing link?

Channels (Austin). 2014;8(1):90-4. doi: 10.4161/chan.27179. Epub 2013 Dec 3.

Authors

Pascal Gosselin-Badaroudine¹, Adrien Moreau¹, Mohamed Chahine²

Affiliations

¹ Centre de recherche; Institut universitaire en santé mentale de Québec; Quebec City, QC Canada.
² Centre de recherche; Institut universitaire en santé mentale de Québec; Quebec City, QC Canada; Department of Medicine; Université Laval; Quebec City, QC Canada.

Abstract

Nav 1.5 dysfunctions are commonly linked to rhythms disturbances that include type 3 long QT syndrome (LQT3), Brugada syndrome (BrS), sick sinus syndrome (SSS) and conduction defects. Recently, this channel protein has been also linked to structural heart diseases such as dilated cardiomyopathy (DCM).

Keywords: Nav1.5; arrhythmias; dilated cardiomyopathy; gating pore; heart; sodium channels; structural model.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Cardiomyopathy, Dilated / genetics*
Cardiomyopathy, Dilated / physiopathology*
Humans
Ion Channel Gating
Mutation
NAV1.5 Voltage-Gated Sodium Channel / physiology*
Phenotype

Substances

NAV1.5 Voltage-Gated Sodium Channel

Abstract

Publication types

MeSH terms

Substances

Grants and funding