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.
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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.