Key result
Endothelial miR-24 inhibition limits infarct size and preserves cardiac function by boosting vascularity in mice.
Why the study?
Does blocking miR-24 improve angiogenesis and reduce infarct size in preclinical models of myocardial infarction?
Comparison
Overexpression or silencing of miR-24 versus blocking endothelial miR-24
Design
Experimental study including cellular assays, zebrafish embryos, and mouse myocardial infarction models
Authors
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miR-24 may regulate post-ischemic angiogenesis in animals; leaves open its therapeutic targeting in human post-MI remodeling.
Does blocking miR-24 improve angiogenesis and reduce infarct size in preclinical models of myocardial infarction?
Blocking miR-24 prevents endothelial apoptosis and enhances angiogenesis, reducing infarct size and preserving cardiac function in preclinical models of myocardial infarction.
Fiedler et al. (2011) studied Myocardial infarction. Blocking of endothelial miR-24 was evaluated on Myocardial infarct size, cardiac function, and survival. Blocking endothelial miR-24 limited myocardial infarct size in mice via prevention of endothelial apoptosis and enhancement of vascularity, leading to preserved cardiac function and survival.
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