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Cystatin C and cathepsins in cardiovascular disease.

Bengtsson, Eva LU ; Nilsson, Jan LU and Jovinge, Stefan LU (2008) In Frontiers in Bioscience 13(1). p.5780-5786
Abstract
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Frontiers in Bioscience
volume
13
issue
1
pages
5780 - 5786
publisher
Frontiers
external identifiers
  • wos:000255885000195
  • pmid:18508621
  • scopus:52049085744
ISSN
1093-9946
language
English
LU publication?
yes
id
39e6fa86-87f3-4f6a-81cb-150afabb5b1b (old id 1153710)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18508621?dopt=Abstract
date added to LUP
2008-06-02 11:00:25
date last changed
2017-03-26 04:25:52
@article{39e6fa86-87f3-4f6a-81cb-150afabb5b1b,
  abstract     = {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.},
  author       = {Bengtsson, Eva and Nilsson, Jan and Jovinge, Stefan},
  issn         = {1093-9946},
  language     = {eng},
  number       = {1},
  pages        = {5780--5786},
  publisher    = {Frontiers},
  series       = {Frontiers in Bioscience},
  title        = {Cystatin C and cathepsins in cardiovascular disease.},
  volume       = {13},
  year         = {2008},
}