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.
| Original language | English |
|---|---|
| Pages (from-to) | 5780-5786 |
| Journal | Frontiers in Bioscience |
| Volume | 13 |
| Issue number | 1 |
| Publication status | Published - 2008 |
Bibliographical note
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)
Subject classification (UKÄ)
- Cardiac and Cardiovascular Systems
- Cell and Molecular Biology
