期刊
JOURNAL OF INTERNAL MEDICINE
卷 263, 期 5, 页码 517-527出版社
WILEY
DOI: 10.1111/j.1365-2796.2008.01965.x
关键词
cathepsin; collagen; extracellular matrix; fibrous cap; matrix metalloproteinase; plaque rupture
资金
- NHLBI NIH HHS [R01 HL080472, HL080472, R01 HL080472-04] Funding Source: Medline
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.
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