Format

Send to

Choose Destination
See comment in PubMed Commons below
Curr Opin Lipidol. 2012 Oct;23(5):439-45. doi: 10.1097/MOL.0b013e32835688e4.

LOX-1: a multiligand receptor at the crossroads of response to danger signals.

Author information

1
Department of Vascular Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan. t-sawamura@umin.ac.jp

Abstract

PURPOSE OF REVIEW:

LOX-1 is a multiligand receptor implicated in endothelial dysfunction and atherosclerosis, although it was originally identified as an oxidized LDL receptor. In this review, the roles of various LOX-1 ligands and their interaction with LOX-1 are discussed to understand the pathophysiological significance of LOX-1.

RECENT FINDINGS:

LOX-1 knockout mice showed resistance of endothelium-dependent vasorelaxation against oxidized LDL and retardation of atherosclerosis progression. LOX-1 ligand reduction in mice also attenuated atherosclerosis progression. In a human cohort study, high concentration of apoB-containing LOX-1 ligands predicted the incidence of cardiovascular disease. Furthermore, modified HDL, which existed in high concentration in the plasma of coronary artery disease patients, was found to induce impairment of endothelial nitric oxide release via LOX-1. In addition to lipoproteins, LOX-1 was found to work as a C-reactive protein receptor providing a scaffold for the activation of the complement system.

SUMMARY:

LOX-1 is a unique molecule among the sensors of danger signals. LOX-1 is not only sensing danger signals such as modified LDL and heat shock protein, but also scaffolding other danger sensors including C-reactive protein and C1q, and directly commanding responses to danger signals by working as a cell adhesion molecule. Via these functions, LOX-1 might work as a surveillance molecule of vascular homeostasis.

PMID:
22777292
DOI:
10.1097/MOL.0b013e32835688e4
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments

    Supplemental Content

    Full text links

    Icon for Wolters Kluwer
    Loading ...
    Support Center