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Arteriosclerosis, Thrombosis, and Vascular Biology
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Published Online
on December 8, 2005

Arteriosclerosis, Thrombosis, and Vascular Biology. 2005
Published online before print December 8, 2005, doi: 10.1161/01.ATV.0000199268.27395.4f
A more recent version of this article appeared on February 1, 2006
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*Smoking

Submitted on September 20, 2005
Accepted on November 28, 2005

Smoking, Metallproteinases, and Vascular Disease

Todd S. Perlstein and Richard T. Lee *

From the Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Cambridge, Mass.

* To whom correspondence should be addressed. E-mail: rlee{at}rics.bwh.harvard.edu.

Abstract--Smoking causes up to 11% of total global cardiovascular deaths. Smoking has numerous effects that may promote atherosclerosis through vascular inflammation and oxidative stress, but the pathogenesis of smoking-related cardiovascular disease remains incompletely understood. The matrix metalloproteinases, a family of endopeptidases that can degrade extracellular matrix components in both physiological and pathophysiological states, play an important role in smoking-associated chronic obstructive pulmonary disease, the second leading cause of smoking attributable mortality. Emerging evidence indicates that the matrix metalloproteinases may also contribute to smoking-related vascular disease. Here we discuss the potential relationship between smoking, matrix metalloproteinases, and acceleration of vascular disease.




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