Abstract
Development and progression of atherosclerosis is a complex pathologic event involving cells from both the arterial vessel wall and the immune system, including monocyte-derived macrophages. Monocytes are recruited to the atherosclerotic lesion via an elaborate process involving adhesion to and migration through the endothelial cell layer and into the arterial wall. Adhesion and migration of monocytes is accompanied by activation/differentiation to tissue macrophages. Once inside the atheroma, macrophages are exposed to many factors which further stimulate the cells. Cytokines, low density lipoproteins, and low oxygen levels (hypoxia; a product of tissue thickening in the absence of neovascularization [1]) are all factors which have profound effects on the state of differentiation, function, and survival of macrophages within the atheroma.
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Judware, R., Yun, J.K., McCormick, T.S., Lapetina, E.G. (1998). Integrin Expression and Macrophage Resistance to Apoptosis in Atherosclerosis. In: Gotto, A.M., Lenfant, C., Paoletti, R., Catapano, A.L., Jackson, A.S. (eds) Multiple Risk Factors in Cardiovascular Disease. Medical Science Symposia Series, vol 12. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5022-4_29
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DOI: https://doi.org/10.1007/978-94-011-5022-4_29
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