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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1153710
- author
- Bengtsson, Eva
LU
; Nilsson, Jan
LU
and Jovinge, Stefan
LU
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Frontiers in Bioscience
- volume
- 13
- issue
- 1
- pages
- 5780 - 5786
- publisher
- Frontiers in Bioscience
- external identifiers
-
- wos:000255885000195
- pmid:18508621
- scopus:52049085744
- ISSN
- 1093-9946
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Cardiology (013242100), Hematopoietic Stem Cell Laboratory (013022012), Experimental Cardiovascular Research Unit (013242110)
- 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
- 2016-04-04 08:04:39
- date last changed
- 2022-01-29 02:59:51
@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 in Bioscience}},
series = {{Frontiers in Bioscience}},
title = {{Cystatin C and cathepsins in cardiovascular disease.}},
url = {{http://www.ncbi.nlm.nih.gov/pubmed/18508621?dopt=Abstract}},
volume = {{13}},
year = {{2008}},
}