Cathepsins and cystatin C in atherosclerosis and obesity

Biochimie. 2010 Nov;92(11):1580-6. doi: 10.1016/j.biochi.2010.04.011. Epub 2010 Apr 24.

Abstract

Given the increasing prevalence of human obesity worldwide, there is an urgent need for a better understanding of the molecular mechanisms linking obesity to metabolic and cardiovascular diseases. Our knowledge is nevertheless limited regarding molecules linking adipose tissue to downstream complications. The importance of cathepsins was brought to light in this context. Through a large scale transcriptomic analysis, our group recently identified the gene encoding cathepsin S as one of the most deregulated gene in the adipose tissue of obese subjects and positively correlated with body mass index. Other members of the cathepsin family are expressed in the adipose tissue, including cathepsin K and cathepsin L. Given their implication in atherogenesis, these proteases could participate into the well established deleterious relationship between enlarged adipose tissue and increased cardiovascular risk. Here, we review the clinical and experimental evidence relevant to the role of cathepsins K, L and S and their most abundant endogenous inhibitor, cystatin C, in atherosclerosis and in obesity.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism
  • Adipose Tissue / pathology
  • Animals
  • Atherosclerosis / enzymology
  • Atherosclerosis / metabolism*
  • Cathepsins / antagonists & inhibitors
  • Cathepsins / deficiency
  • Cathepsins / genetics
  • Cathepsins / metabolism*
  • Cystatin C / deficiency
  • Cystatin C / genetics
  • Cystatin C / metabolism*
  • Gene Knockout Techniques
  • Humans
  • Obesity / drug therapy
  • Obesity / enzymology
  • Obesity / metabolism*
  • Obesity / pathology

Substances

  • Cystatin C
  • Cathepsins