Proprotein convertase subtilisin/kexin type 9 potentially influences cholesterol uptake in macrophages and reverse cholesterol transport

FEBS Lett. 2013 May 2;587(9):1271-4. doi: 10.1016/j.febslet.2013.02.027. Epub 2013 Feb 24.


Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes the degradation of low-density lipoprotein receptor (LDLRs) molecules expressed on the cell surface. Gene inactivation of PCSK9 reduces the areas of atherosclerotic lesions in mice, and the effect is mainly dependent on LDLRs. Furthermore, a positive relationship between PCSK9 and cholesterol accumulation in the wall of the aorta has been established. However, the mechanism remains unknown. As PCSK9 is mainly expressed in atherosclerotic plaque and in the liver, we hypothesize that PCSK9 might increase oxidized LDL uptake and impair macrophage-mediated reverse cholesterol transport, contributing to the development of atherosclerosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biological Transport
  • Cholesterol / metabolism*
  • Foam Cells / cytology
  • Foam Cells / metabolism
  • Humans
  • Intestinal Absorption
  • Liver / metabolism
  • Macrophages / cytology
  • Macrophages / metabolism*
  • Mice
  • Proprotein Convertase 9
  • Proprotein Convertases / metabolism*
  • Serine Endopeptidases / metabolism*


  • Cholesterol
  • PCSK9 protein, human
  • Proprotein Convertase 9
  • Proprotein Convertases
  • Serine Endopeptidases