Evaluation of the Altered Pathophysiological Mechanism of the Human Arg302Gln-PRKAG2 Mutation-Induced Metabolic Cardiomyopathy: Studying the Glucose Metabolism Pathway in a Transgenic Mouse Model
Characterized by excessive myocardial glycogen deposition, cardiac hypertrophy, frequent cardiac arrhythmias and progressive conduction system disease, the PRKAG2 cardiac syndrome stems from a genetic mutation in the γ2-subunit of AMP-activated protein kinase (AMPK). Although functionally diverse,...
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| Language: | en |
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2013
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| Online Access: | http://hdl.handle.net/10393/24045 |