Key result
Overexpression of junctin in transgenic mice led to substantial cardiac remodeling, heart enlargement, bradycardia, atrial fibrillation, and increased fibrosis.
Why the study?
Does overexpression of junctin lead to cardiac remodeling and atrial fibrillation in a transgenic mouse model?
Population
Transgenic mice overexpressing canine junctin under the control of mouse a-myosin heavy chain promoter
Design
Preclinical
Authors
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Junctin overexpression induces cardiac enlargement and arrhythmias in mice; leaves open its role in human heart disease.
Does overexpression of junctin lead to cardiac remodeling and atrial fibrillation in a transgenic mouse model?
Overexpression of junctin in the heart leads to substantial cardiac remodeling, atrial fibrillation, and impaired systolic function in a transgenic mouse model.
Hong et al. (2002) studied Cardiac remodeling and atrial fibrillation. Overexpression of canine junctin was evaluated on Cardiac remodeling, bradycardia, atrial fibrillation, and fibrosis. Overexpression of junctin in transgenic mice led to substantial cardiac remodeling, heart enlargement, bradycardia, atrial fibrillation, and increased fibrosis.
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