Cystatin C and cathepsins in cardiovascular disease.
Författare
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.
Publiceringsår
2008
Språk
Engelska
Sidor
5780-5786
Publikation/Tidskrift/Serie
Frontiers in Bioscience
Volym
13
Issue
1
Länkar
Dokumenttyp
Artikel i tidskrift
Förlag
Frontiers in Bioscience
Ämne
- Cardiac and Cardiovascular Systems
- Cell and Molecular Biology
Status
Published
Forskningsgrupp
- Cardiovascular Research - Immunity and Atherosclerosis
ISBN/ISSN/Övrigt
- ISSN: 1093-9946