Infarct in the Heart: What's MMP-9 Got to Do with It?

Over the past three decades, numerous studies have shown a strong connection between matrix metalloproteinase 9 (MMP-9) levels and myocardial infarction (MI) mortality and left ventricle remodeling and dysfunction. Despite this fact, clinical trials using MMP-9 inhibitors have been disappointing. Th...

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Bibliographic Details
Published in:Biomolecules (Basel, Switzerland) Switzerland), 2021-03, Vol.11 (4), p.491
Main Authors: Becirovic-Agic, Mediha, Chalise, Upendra, Daseke, 2nd, Michael J, Konfrst, Shelby, Salomon, Jeffrey D, Mishra, Paras K, Lindsey, Merry L
Format: Article
Language:English
Subjects:
Cardiomyocytes
Chemokines
Clinical trials
Coronary vessels
Cytokines
DNA methylation
Endothelial cells
extracellular matrix
Fibroblasts
Gelatinase B
Growth factors
Heart
Heart failure
Inflammation
Ischemia
Leukocytes
Low density lipoprotein receptors
macrophage
Matrix metalloproteinase
matrix metalloproteinases
Metalloproteinase
Mortality
Myocardial infarction
neutrophil
Neutrophils
Plasma
remodeling
Review
Vascularization
Veins & arteries
Ventricle
Wound healing
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Summary:Over the past three decades, numerous studies have shown a strong connection between matrix metalloproteinase 9 (MMP-9) levels and myocardial infarction (MI) mortality and left ventricle remodeling and dysfunction. Despite this fact, clinical trials using MMP-9 inhibitors have been disappointing. This review focuses on the roles of MMP-9 in MI wound healing. Infiltrating leukocytes, cardiomyocytes, fibroblasts, and endothelial cells secrete MMP-9 during all phases of cardiac repair. MMP-9 both exacerbates the inflammatory response and aids in inflammation resolution by stimulating the pro-inflammatory to reparative cell transition. In addition, MMP-9 has a dual effect on neovascularization and prevents an overly stiff scar. Here, we review the complex role of MMP-9 in cardiac wound healing, and highlight the importance of targeting MMP-9 only for its detrimental actions. Therefore, delineating signaling pathways downstream of MMP-9 is critical.
ISSN:2218-273X
2218-273X
DOI:10.3390/biom11040491