The Journal of Experimental Medicine
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Published online 10 April 2006 doi:10.1084/jem.20060218
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 4, 813-816
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COMMENTARY

Lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander?

Jay W. Heinecke

J.W.H. is at Department of Medicine, University of Washington School of Medicine, Seattle, WA 98195.

CORRESPONDENCE J.W.H.: heinecke{at}u.washington.edu.


Abstract
Oxidation of low-density lipoprotein (LDL) is thought to contribute to atherosclerosis and cardiovascular disease. Consistent with this idea, the antioxidant drug probucol reduces the risk of restenosis, a form of cardiovascular disease, in humans. However, a new study now suggests that the protective effect of probucol depends not on its ability to inhibit lipid oxidation, but on its ability to induce the stress-induced antiinflammatory enzyme heme oxygenase (HO)-1. This might explain why other antioxidants, such as vitamin E, fail to prevent cardiovascular disease in humans.



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J. Exp. Med. 2006 203: 1117-1127. [Abstract] [Full Text] [PDF]



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