| Article ID | Journal | Published Year | Pages | File Type | 
|---|---|---|---|---|
| 2839818 | Clínica e Investigación en Arteriosclerosis | 2010 | 5 Pages | 
Abstract
												In addition to the role of high-density lipoproteins (HDL) in reverse cholesterol transport, new antiatherogenic mechanisms of HDL have been described in the last 10 years. Two of these mechanisms, which are closely related, are the ability of HDL to prevent lowdensity lipoprotein (LDL) oxidation and its antiinflammatory activity. Some of the antiinflammatory properties of HDL are mediated by the content in some lipids such as non-esterified cholesterol or sphingosin-1-phosphate; however, the main antiinflammatory activity of HDL is exerted by the apolipoproteins (apo) and their associated enzymes. Proteins such as apoA-I, cholesteryl ester transfer protein (CETP), paraoxonase, platelet activator favor-acetylhydrolase (PAF-AH) and apoJ act in a coordinated fashion to transfer lipid peroxides, potent oxidizing agents, ranging from oxidized LDLs to HDLs, capture and degrade these lipid peroxides, generating non-inflammatory products. The relative content of these proteins in the distinct HDL subfractions determines the antiinflammatory potential of each subfraction.
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											Authors
												J.L. Sánchez Quesada, J. Ordóñez Llanos, 
											