IMR Press / FBL / Volume 13 / Issue 15 / DOI: 10.2741/3115

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Cystatin C and cathepsins in cardiovascular disease
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1 Department of Clinical Sciences, Experimental Cardiovascular Research Unit, Lund University, Malmo, Sweden
2 Department of Cardiology, Lund University Hospital, Lund University, Lund and Lund Stem Cell Centre, Lund University, Lund, Sweden

*Author to whom correspondence should be addressed.

Academic Editor: James Cox

Front. Biosci. (Landmark Ed) 2008, 13(15), 5780–5786; https://doi.org/10.2741/3115
Published: 1 May 2008
(This article belongs to the Special Issue Cystatins in health and disease)
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.

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