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Deletion of GSK-3β in mice leads to hypertrophic cardiomyopathy secondary to cardiomyoblast hyperproliferation
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Rusty L. Montgomery, Matthew J. Potthoff, Michael Haberland, Xiaoxia Qi, Satoshi Matsuzaki, Kenneth M. Humphries, James A. Richardson, Rhonda Bassel-Duby, Eric N. Olson
Based on extensive preclinical data, glycogen synthase kinase–3 (GSK-3) has been proposed to be a viable drug target for a wide variety of disease states, ranging from diabetes to bipolar disorder. Since these new drugs, which will be more powerful GSK-3 inhibitors than lithium, may potentially be given to women of childbearing potential, and since it has controversially been suggested that lithium therapy might be linked to congenital cardiac defects, we asked whether GSK-3 family members are required for normal heart development in mice....
J. Clin. Invest. doi:10.1172/JCI36245