SCN5A Variants: Association With Cardiac Disorders

The gene encodes the alpha subunit of the main cardiac sodium channel Na 1.5. This channel predominates inward sodium current (INa) and plays a critical role in regulation of cardiac electrophysiological function. Since 1995, variants have been found to be causatively associated with Brugada syndrom...

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Published inFrontiers in physiology Vol. 9; p. 1372
Main Authors Li, Wenjia, Yin, Lei, Shen, Cheng, Hu, Kai, Ge, Junbo, Sun, Aijun
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 09.10.2018
Subjects
cardiac disorders
cardiac sodium channelopathy
Nav1.5
Physiology
SCN5A
therapeutic potential
Nav1.5
cardiac disorders
SCN5A
therapeutic potential
cardiac sodium channelopathy
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Summary:The gene encodes the alpha subunit of the main cardiac sodium channel Na 1.5. This channel predominates inward sodium current (INa) and plays a critical role in regulation of cardiac electrophysiological function. Since 1995, variants have been found to be causatively associated with Brugada syndrome, long QT syndrome, cardiac conduction system dysfunction, dilated cardiomyopathy, etc. Previous genetic, electrophysiological, and molecular studies have identified the arrhythmic and cardiac structural characteristics induced by variants. However, due to the variation of disease manifestations and genetic background, impact of environmental factors, as well as the presence of mixed phenotypes, the detailed and individualized physiological mechanisms in various -related syndromes are not fully elucidated. This review summarizes the current knowledge of genetic variations in different -related cardiac disorders and the newly developed therapy strategies potentially useful to prevent and treat these disorders in clinical setting.
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Reviewed by: Dan Hu, Renmin Hospital, Wuhan University, China; Flavien Charpentier, INSERM U1087 L'unité de Recherche de l'Institut du Thorax, France
Edited by: Jiashin Wu, University of South Florida, United States
This article was submitted to Cardiac Electrophysiology, a section of the journal Frontiers in Physiology
ISSN:1664-042X
1664-042X
DOI:10.3389/fphys.2018.01372