December 30, 2010Cardiovascular Research
Insights into sick sinus syndrome from an inducible mouse model
Key result
Tamoxifen-induced deletion of cardiac pacemaking cells in mice caused degenerative fibrosis and arrhythmias characteristic of sick sinus syndrome, with only a small increase in mortality.
Population
Genetically engineered mouse lines (ROSA-eGFP-DTA and HCN4-KiT-Cre crossed)
Design
Preclinical
Authors
Discussion
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Overview
New inducible mouse model of sick sinus syndrome now available; leaves open translation to human conduction disease.
Structured PICO
P
Population
Genetically engineered mice crossed to achieve an inducible deletion of cells in the cardiac pacemaking and conduction system.
I
Intervention
Tamoxifen-induced deletion of cells specifically in the cardiac pacemaking and conduction system
O
Outcome
Pathohistological changes (degenerative fibrosis of nodal tissue) and arrhythmic manifestationssurrogate
The generation of an inducible mouse model for sick sinus syndrome provides a new tool to study cardiac conduction diseases and nodal cell ablation.
Cite This Study
Herrmann et al. (2010) studied Sick sinus syndrome. Tamoxifen-induced deletion of cells in the cardiac pacemaking and conduction system was evaluated on Pathohistological changes and arrhythmic manifestations. Tamoxifen-induced deletion of cardiac pacemaking cells in mice caused degenerative fibrosis and arrhythmias characteristic of sick sinus syndrome, with only a small increase in mortality.