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J Intern Med. 2008 May;263(5):517-27. doi: 10.1111/j.1365-2796.2008.01965.x.

The molecular mechanisms of the thrombotic complications of atherosclerosis.

Author information

1
Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. plibby@rics.bwh.harvard.edu

Abstract

Our evolving knowledge of the cellular and molecular mechanisms underlying atherosclerosis has helped uncover the underlying causes behind thrombotic complications of this disease. Most fatal coronary thrombosis result from fibrous cap rupture or superficial erosion. Recent research has established a role for matrix metalloproteinases in the regulation of aspects of plaque structure related to propensity to disrupt and provoke thrombosis. Inflammatory pathways impinge on proteinase activity and aspects of oxidative stress that may favour plaque disruption. Novel molecular imaging strategies may permit visualization of proteinase activity in vivo, providing a new functional window on pathophysiology.

PMID:
18410595
PMCID:
PMC2562742
DOI:
10.1111/j.1365-2796.2008.01965.x
[Indexed for MEDLINE]
Free PMC Article

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