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Article

Prevention of ventricular arrhythmia and calcium dysregulation in a catecholaminergic polymorphic ventricular tachycardia mouse model carrying calsequestrin-2 mutation.

Journal of cardiovascular electrophysiology - 1 Mar 2011

Alcalai Ronny, Wakimoto Hiroko, Arad Michael, Planer David, Konno Tetsuo, Wang Libin, Seidman Jon G, Seidman Christine E, Berul Charles I

Abstract excerpt

BACKGROUND: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a familial arrhythmic syndrome caused by mutations in genes encoding the calcium-regulation proteins cardiac ryanodine receptor (RyR2) or calsequestrin-2 (CASQ2). Mechanistic studies indicate that CPVT is mediated by diastolic Ca(2+) overload and increased Ca(2+) leak through the RyR2 channel, implying that treatment targeting these...

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Identifiers

PMID: 20807279
DOI: 10.1111/j.1540-8167.2010.01877.x
PMCID: PMC3053436

Genes

CASQ2

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

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Prevention of ventricular arrhythmia and calcium dysregulation in a catecholaminergic polymorphic ventricular tachycardia mouse model carrying calsequestrin-2 mutation.PMID 20807279Read ↗

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Na+-dependent SR Ca2+ overload induces arrhythmogenic events in mouse cardiomyocytes with a human CPVT mutation.Semantic proximity Read ↗

Calsequestrin 2 (CASQ2) mutations increase expression of calreticulin and ryanodine receptors, causing catecholaminergic polymorphic ventricular tachycardia.Semantic proximity Read ↗

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Molecular and Electrophysiological Bases of Catecholaminergic Polymorphic Ventricular TachycardiaSemantic proximity Read ↗

Molecular and tissue mechanisms of catecholaminergic polymorphic ventricular tachycardia.Semantic proximity Read ↗

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