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Article

Arrhythmogenesis in a catecholaminergic polymorphic ventricular tachycardia mutation that depresses ryanodine receptor function.

Proceedings of the National Academy of Sciences of the United States of America - 31 Mar 2015

Zhao Yan-Ting, Valdivia Carmen R, Gurrola Georgina B, Powers Patricia P, Willis B Cicero, Moss Richard L, Jalife José, Valdivia Héctor H

Abstract excerpt

Current mechanisms of arrhythmogenesis in catecholaminergic polymorphic ventricular tachycardia (CPVT) require spontaneous Ca(2+) release via cardiac ryanodine receptor (RyR2) channels affected by gain-of-function mutations. Hence, hyperactive RyR2 channels eager to release Ca(2+) on their own appear as essential components of this arrhythmogenic scheme. This mechanism, therefore, appears inadequate to explain...

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Identifiers

PMID: 25775566
DOI: 10.1073/pnas.1419795112
PMCID: PMC4386375

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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