ArticleFrontiers in physiology2012
Mouse Models of SCN5A-Related Cardiac Arrhythmias.
Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 46 citations in OpenAlex.
- Proof of concept for monoclonal antibody therapy in a cellular model of acquired long QT syndrome type 3.American journal of physiology. Heart and circulatory physiology · 2024Article
- Loss of the Atrial Fibrillation-Related Gene,Circulation research · 2023Article
- Modeling long QT syndrome type 2 on-a-chip via in-depth assessment of isogenic gene-edited 3D cardiac tissues.Science advances · 2022Article
- Delayed Ventricular Repolarization and Sodium Channel Current Modification in a Mouse Model of Rett Syndrome.International journal of molecular sciences · 2022Article
- Absolute Quantification of Nav1.5 Expression by Targeted Mass Spectrometry.International journal of molecular sciences · 2022Article
- Extensive identification of genes involved in congenital and structural heart disorders and cardiomyopathy.Nature cardiovascular research · 2022Article
- Article
- Brugada Syndrome: Oligogenic or Mendelian Disease?International journal of molecular sciences · 2020Review
- Transgenic Rabbit Models in Proarrhythmia Research.Frontiers in pharmacology · 2020Review
- Unmasking the molecular link between arrhythmogenic cardiomyopathy and Brugada syndrome.Nature reviews. Cardiology · 2017Review
- The Complex QT/RR Relationship in Mice.Scientific reports · 2016Article
- Brugada syndrome risk loci seem protective against atrial fibrillation.European journal of human genetics : EJHG · 2014Article
- CrossTalk proposal: The late sodium current is an important player in the development of diastolic heart failure (heart failure with a preserved ejection fraction).The Journal of physiology · 2014Article
- Identifying potential functional impact of mutations and polymorphisms: linking heart failure, increased risk of arrhythmias and sudden cardiac death.Frontiers in physiology · 2013Review
- The genetic component of Brugada syndrome.Frontiers in physiology · 2013Article
- Electrophysiological properties of mouse and epitope-tagged human cardiac sodium channel Na v1.5 expressed in HEK293 cells.F1000Research · 2013Article
- Transgenic models of cardiac arrhythmias and sudden death.Frontiers in physiology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations of SCN5A gene, which encodes the α-subunit of the voltage-gated Na(+) channel Na(V)1.5, underlie hereditary cardiac arrhythmic syndromes such as the type 3 long QT syndrome, cardiac conduction diseases, the Brugada syndrome, the sick sinus syndrome, a trial standstill, and numerous overlap syndromes. Patch-clamp studies in heterologous expression systems have provided important information to understand the genotype-phenotype relationships of these diseases. However, they could not clarify how SCN5A mutations can be responsible for such a large spectrum of diseases, for the late age of onset or the progressiveness of some of these diseases and for the overlapping syndromes. Genetically modified mice rapidly appeared as promising tools for understanding the pathophysiological mechanisms of cardiac SCN5A-related arrhythmic syndromes and several mouse models have been established. This review presents the results obtained on these models that, for most of them, recapitulate the clinical phenotypes of the patients. This includes two models knocked out for Nav1.5 β1 and β3 auxiliary subunits that are also discussed. Despite their own limitations that we point out, the mouse models still appear as powerful tools to elucidate the pathophysiological mechanisms of SCN5A-related diseases and offer the opportunity to investigate the secondary cellular consequences of SCN5A mutations such as the expression remodeling of other genes. This points out the potential role of these genes in the overall human phenotype. Finally, they constitute useful tools for addressing the role of genetic and environmental modifiers on cardiac electrical activity.
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