June 27, 2008Circulation ResearchOpen Access

Unexpected Structural and Functional Consequences of the R33Q Homozygous Mutation in Cardiac Calsequestrin

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Population

Homozygous CASQ2(R33Q/R33Q) mouse model of catecholaminergic polymorphic ventricular tachycardia (CPVT)

Design

Preclinical

Authors

NRNicoletta RizziUniversity of Milan NLNian LiuShenyang Pharmaceutical University CNCarlo NapolitanoElectrophysiology

Discussion

Member takes

Implication

Does not yet inform CPVT management; leaves open whether CASQ2-R33Q ultrastructural changes drive human arrhythmias.

Structured PICO

Population

Homozygous CASQ2(R33Q/R33Q) mouse model of catecholaminergic polymorphic ventricular tachycardia (CPVT)

Intervention

Homozygous CASQ2(R33Q/R33Q) mutation

Outcome

Structural and functional consequences including arrhythmia susceptibility, sarcoplasmic reticulum (SR) calcium content, protein levels, and ultrastructural changessurrogate

The CASQ2(R33Q/R33Q) mouse model of CPVT reveals that the mutation leads to reduced CASQ2 content, decreased SR calcium, and ultrastructural abnormalities in the junctional SR.

Cite This Study

Rizzi et al. (2008) studied this question.

synapsesocial.com/papers/6a7a96060b10e55359897802 https://doi.org/10.1161/circresaha.108.171660

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Unexpected Structural and Functional Consequences of the R33Q Homozygous Mutation in Cardiac Calsequestrin

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Unexpected Structural and Functional Consequences of the R33Q Homozygous Mutation in Cardiac Calsequestrin

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider