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Cystatin C and cathepsins in cardiovascular disease.

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Author

Summary, in English

Cystatin C and cathepsins could play a role in almost all processes involved in atherosclerotic lesion formation by their degradation of extracellular matrix proteins and apolipoprotein B100, the protein moiety of LDL. Several cysteine cathepsins are upregulated in human lesions accompanied by a decrease in cystatin C, the major inhibitor of cysteine cathepsins. Recent research show that atherosclerotic mice deficient in cystatin C display increased elastic lamina degradation as well as larger plaque formation. Cathepsin S- and K-deficient atherosclerotic mice, on the other hand, both have less atherosclerosis, where cathepsin S-/- mice exhibited fewer plaque ruptures and cathepsin K-/- larger foam cells than control mice. This article reviews possible roles of cystatin C and cathepsins in different processes and stages of the atherosclerotic disease.

Publishing year

2008

Language

English

Pages

5780-5786

Publication/Series

Frontiers in Bioscience

Volume

13

Issue

1

Document type

Journal article

Publisher

Frontiers in Bioscience

Topic

  • Cardiac and Cardiovascular Systems
  • Cell and Molecular Biology

Status

Published

Research group

  • Cardiovascular Research - Immunity and Atherosclerosis

ISBN/ISSN/Other

  • ISSN: 1093-9946