Why the study?
Does IRAK-M deficiency worsen postinfarction remodeling and systolic dysfunction in a mouse model of myocardial infarction?
Population
Wild-type and IRAK-M(-/-) mice with induced myocardial infarction, and murine cardiac fibroblasts in vitro
Comparison
IRAK-M knockout (IRAK-M(-/-)) vs Wild-type mice
Design
Preclinical
Authors
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IRAK-M may limit adverse post-MI remodeling in mice; leaves open its relevance as a therapeutic target in human heart failure.
Does IRAK-M deficiency worsen postinfarction remodeling and systolic dysfunction in a mouse model of myocardial infarction?
Endogenous IRAK-M protects against adverse postinfarction remodeling by suppressing leukocyte inflammatory activity and inhibiting fibroblast-mediated matrix degradation.
Chen et al. (2012) studied this question.
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