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Review
. 2017:147:75-100.
doi: 10.1016/bs.pmbts.2017.02.001. Epub 2017 Mar 18.

Matrix Metalloproteinases in Myocardial Infarction and Heart Failure

Kristine Y DeLeon-Pennell  1 , Cesar A Meschiari  2 , Mira Jung  2 , Merry L Lindsey  3
Affiliations
Review

Matrix Metalloproteinases in Myocardial Infarction and Heart Failure

Kristine Y DeLeon-Pennell et al. Prog Mol Biol Transl Sci. 2017.

Abstract

Cardiovascular disease is the leading cause of death, accounting for 600,000 deaths each year in the United States. In addition, heart failure accounts for 37% of health care spending. Matrix metalloproteinases (MMPs) increase after myocardial infarction (MI) and correlate with left ventricular dysfunction in heart failure patients. MMPs regulate the remodeling process by facilitating extracellular matrix turnover and inflammatory signaling. Due to the critical role MMPs play during cardiac remodeling, there is a need to better understand the pathophysiological mechanism of MMPs, including the biological function of the downstream products of MMP proteolysis. Future studies developing new therapeutic targets that inhibit specific MMP actions to limit the development of heart failure post-MI are warranted. This chapter focuses on the role of MMPs post-MI, the efficiency of MMPs as biomarkers for MI or heart failure, and the future of MMPs and their cleavage products as targets for prevention of post-MI heart failure.

Keywords: Fibrosis; Heart failure; Inflammation; Matrix metalloproteinases; Myocardial infarction; Omics.

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Figures

Figure 1
Figure 1
Myocardial wound healing is dependent on the balance between extracellular matrix (ECM) breakdown and synthesis. Matrix metalloproteinase (MMPs) are critical during this process as key regulators of inflammation, fibrosis, angiogenesis, and collagen degradation. Optimal scar formation (left) requires (1) appropriate inflammation, (2) fibroblast differentiation, proliferation, and migration to the wound site, (3) suitable angiogenesis, and (4) proper synthesis, cross-linking, and alignment of collagen at the infarct site. Too much or too little of these events will result in insufficient scare formation (right) and can facilitate in the development of heart failure post-myocardial infarction.
Figure 2
Figure 2
Therapeutics given to post-myocardial infarction patients either directly or indirectly inhibit matrix metalloproteinase (MMP) activity leading to extracellular matrix (ECM) remodeling of the left ventricle (LV).
See this image and copyright information in PMC

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