February 25, 2005Circulation Research

Triadin Overexpression Stimulates Excitation-Contraction Coupling and Increases Predisposition to Cellular Arrhythmia in Cardiac Myocytes

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Population

Adult rat ventricular myocytes

Comparison

Adenoviral-mediated overexpression of wild-type… vs Control myocytes

Design

Preclinical

Authors

DTDmitry TerentyevNew Jersey Institute of Technology SCSteven E. CalaWayne State University THTimothy D. HouleWayne State University

Discussion

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Implication

Triadin overexpression may promote cellular arrhythmias via RyR2; leaves open its role in human arrhythmogenesis.

Structured PICO

Population

Adult rat ventricular myocytes

Intervention

Adenoviral-mediated overexpression of wild-type Triadin 1 (TRD(WT)) or a TRD mutant lacking residues 200 to 224 (TRD(Del.200-224))

Comparator

Control myocytes

Outcome

Intracellular Ca signaling (amplitude of I(Ca)-induced Ca transients, frequency of spontaneous Ca sparks, SR Ca content) and RyR2 channel activitysurrogate

Triadin 1 enhances cardiac excitation-contraction coupling by directly stimulating RyR2, and its overexpression predisposes to cellular arrhythmias.

Cite This Study

Terentyev et al. (2005) studied this question.

synapsesocial.com/papers/6a9133fb029b8b7e89fb594e https://doi.org/10.1161/01.res.0000160609.98948.25

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Triadin Overexpression Stimulates Excitation-Contraction Coupling and Increases Predisposition to Cellular Arrhythmia in Cardiac Myocytes

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Triadin Overexpression Stimulates Excitation-Contraction Coupling and Increases Predisposition to Cellular Arrhythmia in Cardiac Myocytes

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider