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https://hdl.handle.net/2440/105101
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Type: | Journal article |
Title: | The role of cholesterol efflux in mechanisms of endothelial protection by HDL |
Author: | Prosser, H. Ng, M. Bursill, C. |
Citation: | Current Opinion in Lipidology, 2012; 23(3):182-189 |
Publisher: | Lippincott Williams & Wilkins |
Issue Date: | 2012 |
ISSN: | 0957-9672 1473-6535 |
Statement of Responsibility: | Hamish C. Prosser, Martin K.C. Ng, and Christina A. Bursill |
Abstract: | Purpose of review: HDL and their main apolipoprotein (apo) constituent apoA-I are antiatherogenic. This has been predominantly attributed to the ability of apoA-I/HDL to efflux cholesterol from macrophages within atherosclerotic plaques. It is now emerging that a number of the protective properties of HDL may be due to their effects on the endothelium. Recent findings: In addition to their well characterized anti-inflammatory and antioxidant effects, apoA-I and HDL regulate several other key biological pathways known to preserve endothelial function and promote vascular repair. The ATP-binding cassette (ABC) transporters ABCA1 and ABCG1, and the scavenger receptor B type 1 mediate multiple intracellular signaling pathways as well as the efflux of cholesterol and/or oxysterols in response to apoA-I/HDL. Although cholesterol efflux triggers a host of signaling events in endothelial cells, there is evidence that some of the beneficial actions of HDL may occur independently of efflux. Summary: Current data suggest that in endothelial cells ABCA1 and ABCG1 mediate the activation of intracellular signaling pathways primarily through the efflux of cholesterol and oxysterols to apoA-I/HDL. Interaction between HDL and scavenger receptor B type 1 initiates the greatest number of known signaling pathways and there is evidence that some of these are activated independent of efflux. |
Keywords: | cholesterol efflux; endothelium; endothelial nitric oxide synthase; HDL; signaling |
Rights: | Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. |
DOI: | 10.1097/MOL.0b013e328352c4dd |
Grant ID: | http://purl.org/au-research/grants/nhmrc/632512 |
Published version: | http://dx.doi.org/10.1097/mol.0b013e328352c4dd |
Appears in Collections: | Aurora harvest 8 Medicine publications |
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