Atherosclerosis involves the slow buildup of fatty substances, cholesterol, collagen and elastin fibers, macrophages, and other molecules in the arterial lining, which results in formation of a plaque that can partially or totally block the flow of blood. It has been previously suggested that macrophages play a key role in inducing plaque rupture as rupture-prone lesions have been shown to be macrophage-rich.
Elaine Raines and colleagues devised a strategy to overexpress matrix metalloproteinase-9 (MMP-9) in the macrophages of advanced atherosclerotic lesions in mice. The authors found that macrophages secreting an autoactivating form of MMP-9 enhanced elastin breakdown in the surrounding extracellular matrix that physically stabilizes the plaque, and consequently induced plaque rupture. MMP-9 and factors that regulate its activation may be potential therapeutic targets for stabilizing rupture-prone plaques.
TITLE: Macrophage expression of active MMP-9 induces acute plaque disruption in apoE-deficient mice
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