Why the study?
Does miR-208a silencing improve cardiac function and reduce apoptosis, fibrosis, and hypertrophy in a mouse model of myocardial infarction?
Population
Cultured neonatal mice myocytes and male C57BL/6 mice subjected to myocardial infarction
Comparison
miR-208a antagomir vs Vehicle only (control group) and sham operation
Design
Preclinical, randomly assigned
Follow-up
28 days
Authors
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Supports miR-208a inhibition in murine post-MI remodeling; leaves open human translation.
Does miR-208a silencing improve cardiac function and reduce apoptosis, fibrosis, and hypertrophy in a mouse model of myocardial infarction?
Silencing miR-208a attenuates apoptosis, fibrosis, and hypertrophy and improves cardiac function in a mouse model of myocardial infarction, suggesting a potential therapeutic target.
Tony et al. (2015) studied this question.
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