Key result
Treatment with the ALK5 inhibitor GW788388 significantly attenuated systolic dysfunction, left ventricular remodeling, and cardiomyocyte hypertrophy (P<0.05) in a rat model of myocardial infarction.
Why the study?
Does GW788388 attenuate left ventricular remodeling and cardiac dysfunction in a rat model of myocardial infarction?
Population
Sprague-Dawley rats with experimental myocardial infarction induced by left anterior descending coronary…
Comparison
GW788388 50 mg.kg.day starting 1 week after… vs Vehicle
Design
Preclinical, randomized
Follow-up
4 weeks
Authors
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Hypothesis-generating for ALK5 inhibition post-MI; leaves open translation to human trials.
RCT
randomized
Does GW788388 attenuate left ventricular remodeling and cardiac dysfunction in a rat model of myocardial infarction?
p-value: p=<0.05
Targeted inhibition of ALK5 signaling with GW788388 attenuates cardiac remodeling and systolic dysfunction following myocardial infarction in a preclinical rat model.
Tan et al. (2010) conducted an RCT in myocardial infarction. GW788388 (ALK5 inhibitor) vs. vehicle was evaluated on systolic dysfunction and left ventricular remodeling (p=<0.05). Treatment with the ALK5 inhibitor GW788388 significantly attenuated systolic dysfunction, left ventricular remodeling, and cardiomyocyte hypertrophy (P<0.05) in a rat model of myocardial infarction.
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