Abstract
High-density lipoproteins (HDL) play an important role in protection against atherosclerosis by mediating reverse cholesterol transport - the transport of excess cholesterol from peripheral tissues to the liver for disposal. SR-BI is a cell surface receptor for HDL and other lipoproteins (LDL and VLDL) and mediates the selective uptake of lipoprotein cholesterol by cells. Overexpression or genetic ablation of SR-BI in mice revealed that it plays an important role in HDL metabolism and reverse cholesterol transport and protects against atherosclerosis in mouse models of the disease. If it plays a similar role in humans then it may be an attractive target for therapeutic intervention. We will review some of the recent advances in the understanding of SR-BI's physiological role and cellular function in lipoprotein metabolism.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Apolipoproteins / metabolism
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Biological Transport
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CD36 Antigens / genetics
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CD36 Antigens / metabolism*
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Carrier Proteins / metabolism
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Cell Line
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Cell Membrane / metabolism
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Cholesterol Ester Transfer Proteins
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Coronary Artery Disease / metabolism*
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Disease Models, Animal
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Glycoproteins*
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Humans
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Lipoproteins, HDL / metabolism*
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Membrane Proteins*
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Mice
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Mice, Transgenic
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Models, Chemical
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Receptors, Immunologic*
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Receptors, Lipoprotein / genetics
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Receptors, Lipoprotein / metabolism*
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Receptors, Scavenger
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Scavenger Receptors, Class B
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Substrate Specificity
Substances
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Apolipoproteins
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CD36 Antigens
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CETP protein, human
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Carrier Proteins
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Cholesterol Ester Transfer Proteins
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Glycoproteins
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Lipoproteins, HDL
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Membrane Proteins
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Receptors, Immunologic
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Receptors, Lipoprotein
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Receptors, Scavenger
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Scarb1 protein, mouse
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Scavenger Receptors, Class B