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Suppression of Atherosclerotic Plaque Progression and Instability by Tissue Inhibitor of Metalloproteinase-2
Author(s) -
Jason L. Johnson,
Andrew H. Baker,
Kazuhiro Oka,
Lawrence Chan,
Andrew C. Newby,
Christopher L. Jackson,
Sarah J. George
Publication year - 2006
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.106.613281
Subject(s) - fibrous cap , lesion , apolipoprotein e , extracellular matrix , medicine , matrix metalloproteinase , tissue inhibitor of metalloproteinase , macrophage , apoptosis , apolipoprotein b , knockout mouse , foam cell , metalloproteinase , pathology , in vitro , cancer research , endocrinology , microbiology and biotechnology , biology , cholesterol , receptor , biochemistry , disease
Matrix metalloproteinase (MMP)-associated extracellular matrix degradation is thought to contribute to the progression and rupture of atherosclerotic plaques. However, direct evidence of this concept remains elusive. We hypothesized that overexpression of tissue inhibitor of metalloproteinase (TIMP)-1 or TIMP-2 would attenuate atherosclerotic plaque development and instability in high fat-fed apolipoprotein E-knockout (apoE(-/-)) mice.

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