Anti-atherogenic mechanisms of high density lipoprotein: effects on myeloid cells.
Anti-atherogenic mechanisms of high density lipoprotein: effects on myeloid cells.
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DOI:
10.1016/j.bbalip.2011.08.003
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发表时间:
2012-03
期刊:
影响因子:
--
通讯作者:
Tall AR
中科院分区:
文献类型:
--
作者:
Murphy AJ;Westerterp M;Yvan-Charvet L;Tall AR
In some settings increasing high density lipoprotein (HDL) levels has been associated with a reduction in experimental atherosclerosis. This has been most clearly seen in apolipoprotein A-I (apoA-I) transgenic mice or in animals infused with HDL or its apolipoproteins. A major mechanism by which these treatments are thought to delay progression or cause regression of atherosclerosis is by promoting efflux of cholesterol from macrophage foam cells. In addition, HDL has been described as having anti-inflammatory and other beneficial effects. Some recent research has linked anti-inflammatory effects to cholesterol efflux pathways but likely multiple mechanisms are involved. Macrophage cholesterol efflux may have a role in facilitating emigration of macrophages from lesions during regression. While macrophages can mediate cholesterol efflux by several pathways, studies in knockout mice or cells point to the importance of active efflux mediated by ATP binding cassette transporter (ABC) A1 and G1. In addition to traditional roles in macrophages, these transporters have been implicated in the control of hematopoietic stem cell proliferation, monocytosis and neutrophilia, as well as activation of monocytes and neutrophils. Thus, HDL and cholesterol efflux pathways may have important anti-atherogenic effects at all stages of the myeloid cell/monocyte/dendritic cell/macrophage lifecycle.
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DOI:
10.4049/jimmunol.0902372
发表时间:
2010-01-01
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Armstrong AJ;Gebre AK;Parks JS;Hedrick CC
通讯作者:
Hedrick CC
影响因子:
20.3
作者:
Gomes, Ana L.;Carvalho, Tania;Dias, Sergio
通讯作者:
Dias, Sergio
影响因子:
30.8
作者:
Bodzioch, M;Orsó, E;Schmitz, G
通讯作者:
Schmitz, G
影响因子:
37.8
作者:
Feig JE;Parathath S;Rong JX;Mick SL;Vengrenyuk Y;Grauer L;Young SG;Fisher EA
通讯作者:
Fisher EA
影响因子:
15.9
作者:
Feig, Jonathan E.;Pineda-Torra, Ines;Fisher, Edward A.
通讯作者:
Fisher, Edward A.