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Updated: Feb 3, 2026

Histological Quantification of Chronic Myocardial Infarct in Rats
Published on: December 11, 2016
Matrix metalloproteinase-12 as an endogenous resolution promoting factor following myocardial infarction
Alan J Mouton1, Osvaldo J Rivera Gonzalez1, Amanda R Kaminski1
1Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 N State St, Jackson, MS, 39216, United States.
Abstract:
Following myocardial infarction (MI), timely resolution of inflammation promotes wound healing and scar formation while limiting excessive tissue damage. Resolution promoting factors (RPFs) are agents that blunt leukocyte trafficking and inflammation, promote necrotic and apoptotic cell clearance, and stimulate scar formation. Previously identified RPFs include mediators derived from lipids (resolvins, lipoxins, protectins, and maresins), proteins (glucocorticoids, annexin A1, galectin 1, and melanocortins), or gases (CO, H2S, and NO). Matrix metalloproteinase-12 (MMP-12; macrophage elastase) has shown promising RPF qualities in a variety of disease states. We review here the evidence that MMP-12 may serve as a novel RPF with potential therapeutic efficacy in the setting of MI.
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