MT1-MMP–Dependent Remodeling of Cardiac Extracellular Matrix Structure and Function Following Myocardial Infarction
Key result
Heterozygous MT1-MMP deficiency improves survival and preserves myocardial function versus wild-type in mice post-MI.
Why the study?
Does MT1-MMP deficiency improve survival and myocardial function following myocardial infarction in a mouse model?
Population
Cardiac explants from mice deficient in MMP-13, MMP-8, MMP-2, MMP-9, or MT1-MMP, and an in vivo experimental…
Comparison
Heterozygous MT1-MMP-null allele vs Wild-type littermates
Design
Preclinical
Authors
Discussion
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Member takes
Implication
MT1-MMP inhibition merits further preclinical testing post-MI; leaves open translation to human outcomes.
Structured PICO
Does MT1-MMP deficiency improve survival and myocardial function following myocardial infarction in a mouse model?
P
Population
Cardiac explants from mice deficient in MMP-13, MMP-8, MMP-2, MMP-9, or MT1-MMP, and an in vivo experimental model of myocardial infarction using mice heterozygous for an MT1-MMP-null allele and wild-type littermates.
E
Exposure
Heterozygous MT1-MMP-null allele (MT1-MMP deficiency)
C
Comparator
Wild-type littermates
O
Outcome
Survival and myocardial function following experimental myocardial infarction
MT1-MMP is identified as the dominant collagenase responsible for postinfarction cardiac extracellular matrix remodeling and subsequent cardiac dysfunction, highlighting it as a potential therapeutic target.
Cite This Study
Koenig et al. (2012) studied Myocardial Infarction. MT1-MMP-null allele heterozygosity vs. Wild-type littermates was evaluated on Survival and myocardial function. Mice heterozygous for an MT1-MMP-null allele displayed a survival advantage and retained myocardial function relative to wild-type littermates following experimental myocardial infarction.