Abstract
An atherosclerotic plaque is characterized by the accumulation of lipids and immune cells, among which macrophages, neutrophils, dendritic cells and T cells, and by the proliferation of vascular smooth muscle cells that produce matrix proteins such as collagen. In turn, macrophages in the plaque produce a number of proteases including matrix metalloproteinases and cathepsins that degrade matrix proteins and thereby destabilize the fibrous cap. Up to a number of years ago, it was generally presumed that intimal proliferative or synthetic smooth muscle cells originate from medial contractile smooth muscle cells, while macrophages differentiate from monocytes that transmigrate through the endothelial layer upon vascular injury [1,2].
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