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Figure 3 Maturation of the atherosclerotic plaque. More mature lesions develop a fibrous cap composed of a dense extracellular matrix containing collagen and elastin. Underneath the fibrous cap, a lipid core forms that contains many macrophages, dead or dying macrophages, cellular debris including apoptotic bodies, and extracellular lipid accumulations. Proinflammatory mediators released from activated white cells and endothelial cells and smooth muscle cells (SMC) can potentiate cell death by apoptosis in the advancing lesion. As SMCs die within lesions, fewer remain to renew the extracellular matrix in the plaque’s fibrous cap. In addition, the activated cells in the lesion, notably the macrophages, secrete proteinases that can degrade the macromolecules of the extracellular matrix. In particular, interstitial collagenases can attack the triple helical collagen fragments, weakening the fibrous cap. Elastases can break down elastin required for migration of cells within the lesion, and arterial remodeling occurs during compensatory enlargement, and in the extreme, aneurysm formation. During this phase of atherogenesis neovessels form in the intima, often arising as extensions of vasa vasorum that originate in the adventitial layer. IEL = internal elastic lamina; MFC = macrophage foam cell; ROS = reactive oxygen species.