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Figure 1 Metabolism of collagen and elastin in the plaque’s fibrous cap. The vascular smooth muscle cell synthesizes the extracellular matrix protein, collagen, and elastin from amino acids. In the unstable plaque, interferon-gamma (IFN-) secreted by activated T cells may inhibit collagen synthesis, interfering with maintenance and repair of the collagenous framework of the fibrous cap. The activated macrophage secretes proteases that can break down both collagen and elastin to peptides and, eventually, amino acids. Breakdown of these structural molecules of the extracellular matrix can weaken the fibrous cap, rendering it more susceptible to rupture and precipitation of an acute coronary syndrome. IFN- secreted by the T lymphocytes can, in turn, activate the macrophage. Plaques also contain other activators of macrophages, including tumor necrosis factor-alpha (TNF-), macrophage colony-stimulating factor (M-CSF), and macrophage chemoattractant protein-1 (MCP-1), among others. IL = interleukin. (Reprinted from Libby P, et al. Am J Cardiol 2000;86 Suppl:3J–9J. Copyright 2000, with permission from Excerpta Medica Inc., and reproduced with permission from the American Heart Association. Libby P, et al. Molecular bases of the acute coronary syndromes. Circulation 1995;91:2844–50.)