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Isoprostanes as Markers of Lipid Peroxidation in Atherosclerosis

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Part of the book series: Current Inflammation Research ((CIRES))

Abstract

Cardiovascular disease is one of the leading causes of morbidity and mortality in the United States. Central to the process of atherogenesis is the uptake of LDL by macrophages resulting in formation of foam cells in the vascular wall. Thus, insights into the mechanism that leads to the uptake of LDL by macrophages are key to understanding the pathogenesis of atherosclerosis. Native LDL is not internalized by macrophages. However, chemical modification of LDL apolipoprotein B-100 converts the LDL into a ligand for scavenger receptors on macrophages, which leads to rapid uptake of the modified LDL (1–3). Because the scavenger pathway of LDL uptake lacks feedback inhibition by intracellular cholesterol content, massive accumulation of modified LDL can occur, resulting in foam cell formation.

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Roberts, L.J., Morrow, J.D. (1999). Isoprostanes as Markers of Lipid Peroxidation in Atherosclerosis. In: Serhan, C.N., Ward, P.A. (eds) Molecular and Cellular Basis of Inflammation. Current Inflammation Research. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-253-1_7

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