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Cardiovascular Research Advance Access originally published online on May 6, 2009
Cardiovascular Research 2009 83(1):5-6; doi:10.1093/cvr/cvp138
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

CD36: promotion from scavenger receptor to mediator of migration?

Clett Erridge*

Department of Cardiovascular Sciences, University of Leicester, Glenfield General Hospital, Leicester LE3 9QP, UK

* Corresponding author. Tel: +44 116 256 3048; fax: +44 116 287 5792. E-mail address: ce55@le.ac.uk

This editorial refers to ‘The role of the scavenger receptor CD36 in regulating mononuclear phagocyte trafficking to atherosclerotic lesions and vascular inflammation’ by D. Harb et al.,10 pp. 42–51.

The first 10% of the full text of this article appears below.

As the migration of circulating monocytes into the arterial intima and their subsequent differentiation into fat-laden foam cells are critical events in the development of atherosclerosis, the molecular mechanisms underpinning these two events have been the focus of much study in recent years. In particular, since the seminal studies of Goldstein et al.1 revealed almost 30 years ago that foam cell formation could be triggered by the uptake of oxidized low-density lipoprotein (oxLDL) by macrophage scavenger receptors in vitro, much interest has been focused on the potential of scavenger receptors to modulate atherosclerosis.

To date, the class B scavenger receptor CD36 has received the most attention in this context since early studies . . . [Full Text of this Article]


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Related Article

The role of the scavenger receptor CD36 in regulating mononuclear phagocyte trafficking to atherosclerotic lesions and vascular inflammation
Diala Harb, Kim Bujold, Maria Febbraio, Martin G. Sirois, Huy Ong, and Sylvie Marleau
Cardiovasc Res 2009 83: 42-51. [Abstract] [Full Text] [PDF]