Roles and regulation of the cardiac sodium channel Na v 1.5: recent insights from experimental studies.

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Serval ID
serval:BIB_2D49427D9E6D
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
Roles and regulation of the cardiac sodium channel Na v 1.5: recent insights from experimental studies.
Journal
Cardiovascular Research
Author(s)
Abriel H.
ISSN
1755-3245[electronic]
Publication state
Published
Issued date
2007
Volume
76
Number
3
Pages
381-389
Language
english
Notes
Journal Article --- Old month value: Dec 1
Abstract
During the past decade, Na(v)1.5, the main voltage-gated Na(+) channel in the heart, has been shown to be involved in many cardiac diseases. Genetic variants in the gene SCN5A, encoding Na(v)1.5, have been linked to various cardiac phenotypes, such as the congenital and acquired long QT syndromes, Brugada syndrome, conduction slowing, sick sinus syndrome, atrial fibrillation, and even cases of dilated cardiomyopathy. This unexpected phenotypic diversity may reflect that Na(v)1.5 is not only restricted to the initiation of the action potential and rapid cardiac conduction, but may also be involved in other, not-yet elucidated, functions. Despite the fact that our understanding of the regulation of expression, localization, and function of Na(v)1.5 is deepening, we are still far from a comprehensive view. Much of our current knowledge has been obtained by carrying out experiments using "cellular expression systems", e.g. host cells expressing exogenous Na(v)1.5. Although very informative, these techniques are limited, in that Na(v)1.5 is not expressed in the physiological cellular environment of a cardiac cell. Recently, however, there have been several studies published which used approaches closer to "normal" or pathological physiology. In an attempt to summarize recently published data, this article will review the phenotypes of genetically-modified mouse strains where Na(v)1.5 expression and activity are directly or indirectly modified, as well as the regulation of Na(v)1.5 function using native cardiac myocytes. Despite obvious limitations, the reviewed studies provide an overview of the complex multi-factorial and multi-protein regulation of Na(v)1.5.
Keywords
Action Potentials, Animals, Heart Conduction System, Humans, Mice, Mice, Knockout, Mice, Transgenic, Models, Animal, Mutation, Myocytes, Cardiac, Sodium Channels
Pubmed
Web of science
Open Access
Yes
Create date
24/01/2008 10:56
Last modification date
25/09/2019 6:08
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