LOX-1, oxidant stress, mtDNA damage, autophagy, and immune response in atherosclerosis

Can J Physiol Pharmacol. 2014 Jul;92(7):524-30. doi: 10.1139/cjpp-2013-0420. Epub 2014 Feb 11.

Abstract

As a major receptor for oxidized low density lipoprotein (ox-LDL), lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is upregulated in many pathophysiological events, including endothelial cell dysfunction and smooth muscle cell growth, as well as monocyte migration and transformation into foam cells, which are present in atherosclerosis and myocardial ischemia. Excessive production of reactive oxygen species (ROS) increases LOX-1 expression, induces mitochondrial DNA damage, and activates autophagy. Damaged mitochondrial DNA that escapes from autophagy induces an inflammatory response. This paper reviews the potential link between LOX-1, mitochondrial DNA damage, autophagy, and immune response in atherosclerosis.

Keywords: ADN mitochondrial; LDL oxydées; LOX-1; atherosclerosis; athérosclérose; autophagie; autophagy; espèce réactive d’oxygène; immunity; immunité; mitochondrial DNA; oxidized LDL; reactive oxygen species.

Publication types

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

MeSH terms

  • Atherosclerosis / immunology*
  • Atherosclerosis / metabolism*
  • Atherosclerosis / pathology
  • Autophagy*
  • DNA Damage*
  • DNA, Mitochondrial / metabolism*
  • Humans
  • Oxidative Stress*
  • Scavenger Receptors, Class E / metabolism*

Substances

  • DNA, Mitochondrial
  • OLR1 protein, human
  • Scavenger Receptors, Class E