The PRKAG2 gene and hypertrophic cardiomyopathy: an energetically imbalanced relationship
Author:
Affiliation:
1. Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, The Netherlands
Funder
European Commission (EC)
Publisher
American Physiological Society
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology
Link
https://www.physiology.org/doi/pdf/10.1152/ajpheart.00316.2017
Reference27 articles.
1. Fatal Infantile Cardiac Glycogenosis with Phosphorylase Kinase Deficiency and a Mutation in the γ2-Subunit of AMP-Activated Protein Kinase
2. Constitutively active AMP kinase mutations cause glycogen storage disease mimicking hypertrophic cardiomyopathy
3. A PRKAG2 mutation causes biphasic changes in myocardial AMPK activity and does not protect against ischemia
4. Mutations in the gamma2 subunit of AMP-activated protein kinase cause familial hypertrophic cardiomyopathy: evidence for the central role of energy compromise in disease pathogenesis
5. Diagnostic, Prognostic, and Therapeutic Implications of Genetic Testing for Hypertrophic Cardiomyopathy
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