Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016;38(5):1851-9.
doi: 10.1159/000443123. Epub 2016 May 9.

LOX-1-Mediated Effects on Vascular Cells in Atherosclerosis

Free article
Review

LOX-1-Mediated Effects on Vascular Cells in Atherosclerosis

Dimitry A Chistiakov et al. Cell Physiol Biochem. 2016.
Free article

Erratum in

  • Erratum.
    [No authors listed] [No authors listed] Cell Physiol Biochem. 2020;54(5):1095. doi: 10.33594/000000297. Cell Physiol Biochem. 2020. PMID: 33112092 No abstract available.

Retraction in

  • Retraction Statement.
    [No authors listed] [No authors listed] Cell Physiol Biochem. 2020;54(4):806. doi: 10.33594/000000268. Cell Physiol Biochem. 2020. PMID: 32853513 No abstract available.

Abstract

In healthy arteries, expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is almost undetectable. However, in proatherogenic conditions, LOX-1 is markedly up-regulated in vascular cells. In atherosclerosis, LOX-1 appears to be the key scavenger receptor for binding oxidized LDL (oxLDL). Notably, a positive feedback exists between LOX-1 and oxLDL. LOX-1 is involved in mediating of proatherosclerotic effects of oxLDL which result in endothelial dysfunction, proinflammatory recruitment of monocytes into the arterial intima, formation of foam cells, apoptosis of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs), as well as in plaque destabilization and rupture. In this review, we consider effects of the LOX-1/oxLDL axis on several types of vascular cells such as ECs, VSMCs, and macrophages.

PubMed Disclaimer

MeSH terms

Substances

LinkOut - more resources