Cystatin C and cathepsins in cardiovascular disease.
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.
Department of Clinical Sciences, Experimental Cardiovascular Research Unit, Lund University, Malmo, Sweden. eva.bengtsson@med.lu.se
Eva
E
Bengtsson
Jan
J
Nilsson
Stefan
S
Jovinge
D000818:Animals; D050197:Atherosclerosis / Q000503:physiopathology; D001775:Blood Circulation / Q000502:physiology*; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D002403:Cathepsins / Q000502:physiology*; D055316:Cystatin C; D015891:Cystatins / Q000502:physiology*; D004195:Disease Models, Animal; D018450:Disease Progression; D006801:Humans; D008264:Macrophages / Q000473:pathology / Q000502:physiology; D009000:Monocytes / Q000473:pathology / Q000502:physiology
C525030:CST3 protein, human; C525031:Cst3 protein, mouse; D055316:Cystatin C; D015891:Cystatins; D002403:Cathepsins