Key result
In vivo silencing of miR-24 by a specific antagomir in an aorta-constricted mouse model prevented the degradation of heart contraction and the transition to decompensated hypertrophy.
Why the study?
Does in vivo silencing of miR-24 by a specific antagomir prevent the transition toward decompensated hypertrophy in an aorta-constricted mouse model?
Population
Aorta-constricted mouse model
Design
Preclinical
Authors
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miR-24 silencing preserves function in murine pressure overload; leaves open translation to human heart failure therapies.
Does in vivo silencing of miR-24 by a specific antagomir prevent the transition toward decompensated hypertrophy in an aorta-constricted mouse model?
Suppression of miR-24 prevents the transition from compensated to decompensated hypertrophy in a mouse model, suggesting a potential early treatment strategy for heart failure.
Li et al. (2013) studied Compensated hypertrophy transitioning to heart failure. miR-24 specific antagomir was evaluated on Degradation of heart contraction and ventricular hypertrophy. In vivo silencing of miR-24 by a specific antagomir in an aorta-constricted mouse model prevented the degradation of heart contraction and the transition to decompensated hypertrophy.
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