This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tall, A. R. Search for Related Content PubMed PubMed Citation Articles by Tall, A. R. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CHOLESTEROL Related Collections Role of ABCA1 in Cellular Cholesterol Efflux and Reverse Cholesterol Transport

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:710.)
© 2003 American Heart Association, Inc.

ATVB In Focus

ATVB In Focus

Role of ABCA1 in Cellular Cholesterol Efflux and Reverse Cholesterol Transport

Alan R. Tall

From the Division of Molecular Medicine, Department of Medicine, Columbia University, New York.

Correspondence to Dr Alan R. Tall, Columbia University, College of Physicians and Surgeons, 630 West 168th St, New York, NY 10032. E-mail art1@columbia.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

About 30 years ago, John Glomset¹ outlined the reverse cholesterol transport hypothesis, proposing that HDL and LCAT might have anti-atherogenic functions related to their ability to transport cholesterol from peripheral tissues to the liver for excretion. As the different molecules and pathways mediating the various steps of reverse cholesterol transport have been discovered, this hypothesis has been sustained and refined. Much remains to be learned, particularly in relation to molecular mechanisms, regulation, and metabolic integration of the different steps of reverse cholesterol transport. The plot is already thick but undoubtedly there are many new molecular players waiting in the wings. A particular challenge is to manipulate reverse cholesterol transport therapeutically in a way that will reduce atherosclerosis and its complications.

See pages 712 and 720

This review series has been inspired by the discovery in 1999 by three different laboratories (led by Bodzioch et al,² Rust et al,³ and Brooks-Wilson et al⁴) that Tangier Disease is caused by mutations in the ATP binding cassette transporter ABCA1, providing a new molecular key to understanding the mechanisms and regulation of cellular cholesterol efflux. In the first piece in the series, Yancey and colleagues⁵ from the Rothblat and Philips laboratory will describe three different pathways that may mediate cellular cholesterol efflux: aqueous diffusion, scavenger receptor BI (SR-BI)–mediated efflux, and active cholesterol efflux mediated by ABCA1. Their review will discuss in detail various potential mechanisms that may be responsible for cholesterol efflux mediated by SR-BI or ABCA1, and the potential metabolic integration of . . . [Full Text of this Article]

This article has been cited by other articles:

				U. Maitra, J. S. Parks, and L. Li An Innate Immunity Signaling Process Suppresses Macrophage ABCA1 Expression through IRAK-1-Mediated Downregulation of Retinoic Acid Receptor {alpha} and NFATc2 Mol. Cell. Biol., November 15, 2009; 29(22): 5989 - 5997. [Abstract] [Full Text] [PDF]

				R. Movva and D. J. Rader Laboratory Assessment of HDL Heterogeneity and Function Clin. Chem., May 1, 2008; 54(5): 788 - 800. [Abstract] [Full Text] [PDF]

				M.-D. Wang, V. Franklin, and Y. L. Marcel In Vivo Reverse Cholesterol Transport From Macrophages Lacking ABCA1 Expression Is Impaired Arterioscler Thromb Vasc Biol, August 1, 2007; 27(8): 1837 - 1842. [Abstract] [Full Text] [PDF]

				K. Anwar, H. J. Kayden, and M. M. Hussain Transport of vitamin E by differentiated Caco-2 cells J. Lipid Res., June 1, 2006; 47(6): 1261 - 1273. [Abstract] [Full Text] [PDF]

				N. H. Pipalia, A. Huang, H. Ralph, M. Rujoi, and F. R. Maxfield Automated microscopy screening for compounds that partially revert cholesterol accumulation in Niemann-Pick C cells J. Lipid Res., February 1, 2006; 47(2): 284 - 301. [Abstract] [Full Text] [PDF]

				G. S. Shelness and L. L. Rudel A Role for the Pregnane X Receptor in High-Density Lipoprotein Metabolism Arterioscler Thromb Vasc Biol, October 1, 2005; 25(10): 2016 - 2017. [Full Text] [PDF]

				A. Daugherty, N. R. Webb, D. L. Rateri, and V. L. King Thematic review series: The Immune System and Atherogenesis. Cytokine regulation of macrophage functions in atherogenesis J. Lipid Res., September 1, 2005; 46(9): 1812 - 1822. [Abstract] [Full Text] [PDF]

				L. Krimbou, H. Hajj Hassan, S. Blain, S. Rashid, M. Denis, M. Marcil, and J. Genest Biogenesis and speciation of nascent apoA-I-containing particles in various cell lines J. Lipid Res., August 1, 2005; 46(8): 1668 - 1677. [Abstract] [Full Text] [PDF]

				J. Iqbal and M. M. Hussain Evidence for multiple complementary pathways for efficient cholesterol absorption in mice J. Lipid Res., July 1, 2005; 46(7): 1491 - 1501. [Abstract] [Full Text] [PDF]

				M. Walter, N. R. Forsyth, W. E. Wright, J. W. Shay, and M. G. Roth The Establishment of Telomerase-immortalized Tangier Disease Cell Lines Indicates the Existence of an Apolipoprotein A-I-inducible but ABCA1-independent Cholesterol Efflux Pathway J. Biol. Chem., May 14, 2004; 279(20): 20866 - 20873. [Abstract] [Full Text] [PDF]