Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Normal interventricular differences in tissue architecture underlie right ventricular susceptibility to conduction abnormalities in a mouse model of Brugada syndrome.

Cardiovascular research - 1 Apr 2018

Kelly Allen, Salerno Simona, Connolly Adam, Bishop Martin, Charpentier Flavien, Stølen Tomas, Smith Godfrey L

Abstract excerpt

Aims: Loss-of-function of the cardiac sodium channel NaV1.5 is a common feature of Brugada syndrome. Arrhythmias arise preferentially from the right ventricle (RV) despite equivalent NaV1.5 downregulation in the left ventricle (LV). The reasons for increased RV sensitivity to NaV1.5 loss-of-function mutations remain unclear. Because ventricular electrical activation occurs predominantly in the transmural axis, we...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Action Potentials
Share to Brugada Syndrome

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Disease Models, Animal

Share to Genetic Predisposition to Disease

Share to Mice, Knockout

Share to NAV1.5 Voltage-Gated Sodium Channel

Share to Phenotype

Share to Time Factors

Source

Open in PubMed Open full text

Identifiers

PMID: 29267949
DOI: 10.1093/cvr/cvx244
PMCID: PMC5915948

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Normal interventricular differences in tissue architecture underlie right ventricular susceptibility to conduction abnormalities in a mouse model of Brugada syndrome.PMID 29267949Read ↗

Genetic background determines the severity of age-dependent cardiac structural abnormalities and arrhythmia susceptibility in Scn5a-1798insD mice.Semantic proximity Read ↗

The Brugada syndrome associated gene <i>WT1</i> impacts on <i>SCN5A</i> expression and cardiac conductionSemantic proximity Read ↗

Genetically determined differences in sodium current characteristics modulate conduction disease severity in mice with cardiac sodium channelopathy.Semantic proximity Read ↗

Slowed conduction and ventricular tachycardia after targeted disruption of the cardiac sodium channel gene Scn5a.Semantic proximity Read ↗

In vivo studies of Scn5a+/- mice modeling Brugada syndrome demonstrate both conduction and repolarization abnormalities.Semantic proximity Read ↗

Delayed conduction and its implications in murine Scn5a(+/-) hearts: independent and interacting effects of genotype, age, and sex.Semantic proximity Read ↗

Variable Na(v)1.5 protein expression from the wild-type allele correlates with the penetrance of cardiac conduction disease in the Scn5a(+/-) mouse model.Semantic proximity Read ↗

Non-canonical Sodium Channel Isoforms Underlie Chamber Specific Cardiac ExcitabilitySemantic proximity Read ↗

Scn2b Deletion in Mice Results in Ventricular and Atrial Arrhythmias.Semantic proximity Read ↗

Genetic mouse models of autism spectrum disorder present subtle heterogenous cardiac abnormalities.Semantic proximity Read ↗

Prolonged Right Ventricular Ejection Delay in Brugada Syndrome Depends on the Type of SCN5A Variant - Electromechanical Coupling Through Tissue Velocity Imaging as a Bridge Between Genotyping and Phenotyping.Semantic proximity Read ↗

Loss of Nav1.5 expression and function in murine atria containing the RyR2-P2328S gain-of-function mutation.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.