CD36 modulation in the subintimal trapping and LDL-mediated migration of macrophages

Abstract

Evaluation of: Park YM, Febbraio M, Silverstein RL. CD36 modulates migration of mouse and human macrophages in response to oxidized LDL and may contribute to macrophage trapping in the arterial intima. J. Clin. Invest. 119, 136–145 (2009).

Atherosclerosis is an immune-mediated chronic inflammatory disease and the leading cause of death in developed countries. It is characterized by the subintimal deposition of oxidized LDL, which triggers a cascade of inflammatory reactions resulting in the formation of atheromatous plaques, narrowing the arterial lumen and, on rupture, leading to thrombotic complications. Macrophages are a central part of this process, their primary role being the phagocytosis of the LDL particles. However, once this has been accomplished, the macrophages can remain resident in the atheroma, rather than leaving it. This leads to progression of the atherosclerotic plaques. The paper discussed has identified a possible mechanism responsible for trapping macrophages within the intima. This may have significant clinical implications since, by blocking this process, reversal of the atherosclerotic process may be possible.

Keywords::

• arterial intima
• atherosclerosis
• CD36
• macrophage
• migration
• oxidized LDL

Financial & competing interests disclosure

Umar Sadat is funded by Medical Research Council (UK) and Royal College of Surgeons of England joint clinical research training fellowship. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.