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. Author manuscript; available in PMC: 2016 Feb 7.
Published in final edited form as: Annu Rev Nutr. 2015;35:517–543. doi: 10.1146/annurev-nutr-071714-034449

Figure 2.

Figure 2

Low-density lipoprotein (LDL) particles and atherogenesis. In the initial steps of atherogenesis, LDL particles circulating in the blood infiltrate the endothelial layer of arteries and are bound by proteoglycans and become oxidized. This triggers inflammatory processes and foam cell formation by responding macrophages. These lipid-laden foam cells form the core of the atherosclerotic plaque and can amplify local inflammation and promote thrombosis. Apolipoprotein CIII (apoCIII), an exchangeable apoprotein whose concentrations vary on apoB-containing particles, has been shown to play a direct role in some of these processes. Small, dense LDL is considered more atherogenic due to its longer plasma residence time, higher apoCIII content, greater arterial retention, and increased susceptibility to oxidation, triggering inflammatory and thrombotic processes. Abbreviation: oxLDL, oxidized LDL.