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October 15, 2008Journal of Clinical InvestigationOpen Access

Deletion of GSK-3β in mice leads to hypertrophic cardiomyopathy secondary to cardiomyoblast hyperproliferation

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Population

Gsk3b(-/-) embryoid bodies, GSK-3alpha-deficient mice, and Gsk3b(-/-) embryos/pups

Design

Preclinical

Authors

RKRisto KerkeläHeart Failure / CardiomyopathyLKLisa KockeritzUniversity of TorontoKMKatrina MacAulayUnilever (United Kingdom)

Discussion

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Implication

GSK-3 inhibition may carry teratogenic risks in pregnancy; animal data leave open translation to humans and clinical use.

Structured PICO

P
Population
Gsk3b(-/-) embryoid bodies, GSK-3alpha-deficient mice, and Gsk3b(-/-) embryos/pups
I
Intervention
Genetic deletion of GSK-3alpha or GSK-3beta (loss-of-function approach)
O
Outcome
Cardiac development, cardiomyocyte differentiation, and embryonic viabilitysurrogate

GSK-3beta is a central regulator of embryonic cardiomyocyte proliferation and differentiation, suggesting that pharmacological inhibition of GSK-3 may carry teratogenic risks.

Cite This Study

Kerkelä et al. (2008) studied this question.

synapsesocial.com/papers/6a761e410327049ca48c5b92https://doi.org/10.1172/jci36245

Topics

Hypertrophic cardiomyopathy
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