on September 4, 2008
Published online before print September 4, 2008, doi: 10.1161/ATVBAHA.108.173898
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Submitted on December 4, 2007
Accepted on August 25, 2008
Metalloproteinase Expression in Monocytes and Macrophages and its Relationship to Atherosclerotic Plaque Instability
Andrew C. Newby *
From the Bristol Heart Institute, University of Bristol, UK.
* To whom correspondence should be addressed. E-mail: A.Newby{at}bris.ac.uk.
Abstract—Matrix metalloproteinases (MMPs) can degrade strength-giving collagens and other structural proteins of the arterial extracellular matrix. Overproduction of MMPs by monocyte/macrophages could therefore promote atherosclerotic plaque rupture and myocardial infarction. Freshly-recruited monocyte macrophages appear to use a prostaglandin (PG)-dependent pathway to coordinately upregulate a broad and potentially highly-destructive spectrum of MMPs. Differentiated macrophages rely on a series of distinct pathways to selectively upregulate groups of MMPs. Moreover, recent evidence suggests that different macrophage phenotypes express characteristically different spectra of MMPs and their inhibitors. New therapies may result from targeting matrix MMP overproduction.
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