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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:250.)
© 2006 American Heart Association, Inc.

Brief Reviews

Smoking, Metalloproteinases, and Vascular Disease

Todd S. Perlstein; Richard T. Lee

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

Correspondence to Richard T. Lee, Cardiovascular Research Laboratories, Partners Research Facility, 65 Landsdowne St., Room 279, Cambridge, MA 02139. E-mail rlee{at}rics.bwh.harvard.edu

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.

The matrix metalloproteinases are emerging as strong candidate mediators of smoking-associated vascular disease. Smoking-induced inflammation and oxidative stress may increase metalloproteinase transcription, increase pro-enzyme activation, and limit endogenous inhibition of metalloproteinase activity. The relationship between smoking, metalloproteinases, and vascular disease is discussed in this brief review.

Key Words: vascular disease • smoking • metalloproteinases

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