Journal
PHYSIOLOGY
Volume 28, Issue 6, Pages 391-403Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physiol.00029.2013
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Funding
- NIH/NHLBI HHSN [268201000036C (N01-HV-00244), HL-051971, R01 HL-075360]
- Biomedical Laboratory Research and Development Service of the Veterans Affairs Office [5I01BX000505]
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Matrix metalloproteinase (MMP)-9, one of the most widely investigated MMPs, regulates pathological remodeling processes that involve inflammation and fibrosis in cardiovascular disease. MMP-9 directly degrades extracellular matrix (ECM) proteins and activates cytokines and chemokines to regulate tissue remodeling. MMP-9 deletion or inhibition has proven overall beneficial in multiple animal models of cardiovascular disease. As such, MMP-9 expression and activity is a common end point measured. MMP-9 cell-specific overexpression, however, has also proven beneficial and highlights the fact that little information is available on the underlying mechanisms of MMP-9 function. In this review, we summarize our current understanding of MMP-9 physiology, including structure, regulation, activation, and downstream effects of increased MMP-9. We discuss MMP-9 roles during inflammation and fibrosis in cardiovascular disease. By concentrating on the substrates of MMP-9 and their roles in cardiovascular disease, we explore the overall function and discuss future directions on the translational potential of MMP-9 based therapies.
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