Cystatin C and cathepsins in cardiovascular disease.

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Cystatin C and cathepsins in cardiovascular disease. / Bengtsson, Eva; Nilsson, Jan; Jovinge, Stefan.

In: Frontiers in Bioscience, Vol. 13, No. 1, 2008, p. 5780-5786.

Research output: Contribution to journalArticle

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TY - JOUR

T1 - Cystatin C and cathepsins in cardiovascular disease.

AU - Bengtsson, Eva

AU - Nilsson, Jan

AU - Jovinge, Stefan

N1 - 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)

PY - 2008

Y1 - 2008

N2 - 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.

AB - 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.

M3 - Article

VL - 13

SP - 5780

EP - 5786

JO - Frontiers

T2 - Frontiers

JF - Frontiers

SN - 1093-9946

IS - 1

ER -