Cystatin C and cathepsins in cardiovascular disease.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

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.

Detaljer

Författare
Enheter & grupper
Forskningsområden

Ämnesklassifikation (UKÄ) – OBLIGATORISK

  • Kardiologi
  • Cell- och molekylärbiologi
Originalspråkengelska
Sidor (från-till)5780-5786
TidskriftFrontiers in Bioscience
Volym13
Utgivningsnummer1
StatusPublished - 2008
PublikationskategoriForskning
Peer review utfördJa