ArticleOpen biology2012
Reduced Na(+) and higher K(+) channel expression and function contribute to right ventricular origin of arrhythmias in Scn5a+/- mice.
Article in Open biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Mannitol and hyponatremia regulate cardiac ventricular conduction in the context of sodium channel loss of function.American journal of physiology. Heart and circulatory physiology · 2024Article
- Brugada Syndrome: Different Experimental Models and the Role of Human Cardiomyocytes From Induced Pluripotent Stem Cells.Journal of the American Heart Association · 2022Review
- Transcriptional profiles of genes related to electrophysiological function in Scn5aPhysiological reports · 2021Article
- Dispersion of ventricular repolarization: Temporal and spatial.World journal of cardiology · 2020Review
- Transcriptional and Epigenetic Regulation of Cardiac Electrophysiology.Pediatric cardiology · 2019Review
- Autonomic modulation of the electrical substrate in mice haploinsufficient for cardiac sodium channels: a model of the Brugada syndrome.American journal of physiology. Cell physiology · 2019Article
- Experimental Models of Brugada syndrome.International journal of molecular sciences · 2019Review
- Reduced cardiomyocyte NaJournal of cellular physiology · 2019Article
- Ventricular pro-arrhythmic phenotype, arrhythmic substrate, ageing and mitochondrial dysfunction in peroxisome proliferator activated receptor-γ coactivator-1β deficient (Pgc-1βMechanisms of ageing and development · 2018Article
- Normal interventricular differences in tissue architecture underlie right ventricular susceptibility to conduction abnormalities in a mouse model of Brugada syndrome.Cardiovascular research · 2018Article
- Multiple targets for flecainide action: implications for cardiac arrhythmogenesis.British journal of pharmacology · 2018Review
- Epac-induced ryanodine receptor type 2 activation inhibits sodium currents in atrial and ventricular murine cardiomyocytes.Clinical and experimental pharmacology & physiology · 2018Article
- Cardiomyocyte ionic currents in intact young and aged murine Pgc-1βMechanisms of ageing and development · 2018Article
- Sodium channel biophysics, late sodium current and genetic arrhythmic syndromes.Pflugers Archiv : European journal of physiology · 2017Review
- Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Physiological reviews · 2017Review
- Patient-Specific and Genome-Edited Induced Pluripotent Stem Cell-Derived Cardiomyocytes Elucidate Single-Cell Phenotype of Brugada Syndrome.Journal of the American College of Cardiology · 2016Article
- Differences in Left Versus Right Ventricular Electrophysiological Properties in Cardiac Dysfunction and Arrhythmogenesis.Arrhythmia & electrophysiology review · 2016Article
- Arrhythmic substrate, slowed propagation and increased dispersion in conduction direction in the right ventricular outflow tract of murine Scn5a+/- hearts.Acta physiologica (Oxford, England) · 2014Article
- Action potential wavelength restitution predicts alternans and arrhythmia in murine Scn5a(+/-) hearts.The Journal of physiology · 2013Article
- Andrew Fielding Huxley (1917-2012).The Journal of physiology · 2012Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Brugada syndrome (BrS) is associated with ventricular tachycardia originating particularly in the right ventricle (RV). We explore electrophysiological features predisposing to such arrhythmic tendency and their possible RV localization in a heterozygotic Scn5a+/- murine model. Na(v)1.5 mRNA and protein expression were lower in Scn5a+/- than wild-type (WT), with a further reduction in the RV compared with the left ventricle (LV). RVs showed higher expression levels of K(v)4.2, K(v)4.3 and KChIP2 in both Scn5a+/- and WT. Action potential upstroke velocity and maximum Na(+) current (I(Na)) density were correspondingly decreased in Scn5a+/-, with a further reduction in the RV. The voltage dependence of inactivation was shifted to more negative values in Scn5a+/-. These findings are predictive of a localized depolarization abnormality leading to slowed conduction. Persistent Na(+) current (I(pNa)) density was decreased in a similar pattern to I(Na). RV transient outward current (I(to)) density was greater than LV in both WT and Scn5a+/-, and had larger time constants of inactivation. These findings were also consistent with the observation that AP durations were smallest in the RV of Scn5a+/-, fulfilling predictions of an increased heterogeneity of repolarization as an additional possible electrophysiological mechanism for arrhythmogenesis in BrS.
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Registered trials
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