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The Role of Adhesion Molecules and Intimal Dendritic Cells in the Initiation of Atherosclerosis

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Inflammation and Atherosclerosis

Abstract

The initiation of atherosclerosis in animal models involves development of small fatty streaks that subsequently expand and coalesce. With time, atherosclerotic lesions progress into fibro-fatty plaques with intimal smooth muscle cells, a collagen-rich fibrous cap and a necrotic core. These lesions resemble many features of human atherosclerosis. In advanced vulnerable human plaques, rupture or erosion leads to mural thrombosis, which results in tissue ischemia or infarction (reviewed in [1, 2]). Organization of non-occlusive mural thrombi may also be an important mechanism for plaque growth. It has been known for many years that the recruitment of blood monocytes to the arterial intima is a feature of early as well as advanced atherosclerotic lesions [3, 4]. Monocytes contribute to the growth and expansion of early lesions, where they transform into macrophages, engulf lipids and become foam cells. In advanced lesions, recruited monocytes may also directly participate in plaque destabilization, resulting in thrombotic complications.

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Correspondence to Myron I. Cybulsky .

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Jongstra-Bilen, J., Cybulsky, M.I. (2012). The Role of Adhesion Molecules and Intimal Dendritic Cells in the Initiation of Atherosclerosis. In: Wick, G., Grundtman, C. (eds) Inflammation and Atherosclerosis. Springer, Vienna. https://doi.org/10.1007/978-3-7091-0338-8_7

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