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June 1, 2010Journal of Clinical InvestigationOpen Access

GSK-3α directly regulates β-adrenergic signaling and the response of the heart to hemodynamic stress in mice

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Why the study?

Does GSK-3alpha deletion or inhibition impair beta-adrenergic signaling and the response to hemodynamic stress in mice?

Population

Gsk3a mice over 2 months of age, young mice subjected to thoracic aortic constriction, and WT cardiomyocytes

Comparison

Gsk3a gene knockout and acute treatment with a… vs Wild-type mice and untreated WT cardiomyocytes

Design

Preclinical

Authors

JZJibin ZhouHLHind LalXCXiongwen Chen

Discussion

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Overview

May warrant caution for GSK-3 inhibitors; hypothesis-generating in mice, requires human validation.

Structured PICO

Does GSK-3alpha deletion or inhibition impair beta-adrenergic signaling and the response to hemodynamic stress in mice?

P
Population
Gsk3a(-/-) mice over 2 months of age, young mice subjected to thoracic aortic constriction, and WT cardiomyocytes
I
Intervention
Gsk3a gene knockout and acute treatment with a small molecule GSK-3 inhibitor
C
Comparator
Wild-type (WT) mice and untreated WT cardiomyocytes
O
Outcome
Cardiac hypertrophy, contractile dysfunction, and beta-adrenergic responsivenesssurrogate

GSK-3alpha is a critical regulator of beta-adrenergic signaling and cardiac adaptation to stress, suggesting potential cardiotoxicity for drugs targeting GSK-3.

Cite This Study

Zhou et al. (2010) studied this question.

synapsesocial.com/papers/6a0fe14e2badbc352afee05ahttps://doi.org/10.1172/jci41407
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Also Consider

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  3. 3Constitutive glycogen synthase kinase-3α/β activity protects against chronic β-adrenergic remodelling of the heart2010 · 31 citations
  4. 4Glycogen Synthase Kinase-3β Regulates Post–Myocardial Infarction Remodeling and Stress-Induced Cardiomyocyte Proliferation In Vivo2010 · 120 citations
  5. 5The GSK-3 Family as Therapeutic Target for Myocardial Diseases2014 · 209 citations