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
Loading...
May warrant caution for GSK-3 inhibitors; hypothesis-generating in mice, requires human validation.
Does GSK-3alpha deletion or inhibition impair beta-adrenergic signaling and the response to hemodynamic stress in mice?
GSK-3alpha is a critical regulator of beta-adrenergic signaling and cardiac adaptation to stress, suggesting potential cardiotoxicity for drugs targeting GSK-3.
Zhou et al. (2010) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: