Key result
Cardiomyocyte-specific deletion of GSK-3beta protected against post-MI remodeling, preserving left ventricular function at up to 8 weeks, and promoted stress-induced cardiomyocyte proliferation.
Why the study?
Does inducible, cardiomyocyte-specific deletion of GSK-3beta improve post-MI remodeling and cardiomyocyte proliferation in adult mice?
Population
Adult mice subjected to pressure overload (thoracic aortic constriction) or myocardial infarction
Comparison
Inducible, cardiomyocyte-specific deletion of… vs Control mice with intact GSK-3beta (implied)
Design
Preclinical
Follow-up
up to 8 weeks post-MI
Authors
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:* Identifies GSK-3beta as a potential therapeutic target for post-MI cardiac regeneration.
Does inducible, cardiomyocyte-specific deletion of GSK-3beta improve post-MI remodeling and cardiomyocyte proliferation in adult mice?
Cardiomyocyte-specific deletion of GSK-3beta in adult mice protects against post-MI remodeling and promotes stress-induced cardiomyocyte proliferation, suggesting a potential therapeutic target for cardiac regeneration.
Woulfe et al. (2010) studied Myocardial Infarction and Pressure Overload. Cardiomyocyte-specific deletion of GSK-3beta was evaluated on Hypertrophic response, post-MI remodeling, and cardiomyocyte proliferation. Cardiomyocyte-specific deletion of GSK-3beta protected against post-MI remodeling, preserving left ventricular function at up to 8 weeks, and promoted stress-induced cardiomyocyte proliferation.
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