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Mediators Inflamm. 2013;2013:761789. doi: 10.1155/2013/761789. Epub 2013 Aug 13.

Oxidized LDL and LOX-1 in experimental sepsis.

Author information

1
Department of Anesthesia, Pain Management and Perioperative Medicine, Dalhousie University Halifax, Nova Scotia, Canada B3H 2Y9.

Abstract

Oxidized low-density lipoproteins (oxLDL) and the lectin-like oxLDL receptor-1 (LOX-1) are upregulated in inflammation. Because of the importance of inflammation and capillary leakage in the impairment of the microcirculation, which in turn contributes to the development of sepsis and multiorgan failure, the role of oxidized LDL and LOX-1 as players of intestinal inflammation is of great interest. In fact, the blockade of LOX-1 during experimental endotoxemia was effective in reducing leukocyte activation. There are several mechanisms by which oxLDL can participate in local and systemic inflammation, including cell proliferation, apoptosis, capillary perfusion, leukocyte-endothelial cell interactions, and endothelial activation. This review highlights the evidence relating oxLDL and LOX-1 to proinflammatory disease mechanisms. We also indicate situations when oxLDL, because of exposure time, dose, or degree of oxidization, is involved in disease resolution. Modulation of LOX-1 response could be utilized for the treatment of local and systemic inflammation, but the successful use of this target requires further understanding of its broad effects.

PMID:
24000272
PMCID:
PMC3755390
DOI:
10.1155/2013/761789
[Indexed for MEDLINE]
Free PMC Article

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