Journal
PROGRESS IN LIPID RESEARCH
Volume 52, Issue 4, Pages 446-464Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.plipres.2013.06.001
Keywords
Triglyceride-rich lipoproteins; Postprandial lipemia; Inflammation; Endothelial cells; Monocytes; Macrophages
Funding
- British Heart Foundation
- BBSRC Diet and Health Research Industry Club [BB/1005862/1]
- Biotechnology and Biological Sciences Research Council [BB/I005862/1] Funding Source: researchfish
- BBSRC [BB/I005862/1] Funding Source: UKRI
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Blood levels of triglyceride-rich lipoproteins (TRL) increase postprandially, and a delay in their clearance results in postprandial hyperlipidemia, an important risk factor in atherosclerosis development. Atherosclerosis is a multifactorial inflammatory disease, and its initiation involves endothelial dysfunction, invasion of the artery wall by leukocytes and subsequent formation of foam cells. TRL are implicated in several of these inflammatory processes, including the formation of damaging free radicals, leukocyte activation, endothelial dysfunction and foam cell formation. Recent studies have provided insights into the mechanisms of uptake and the signal transduction pathways mediating the interactions of TRL with leukocytes and vascular cells, and how they are modified by dietary lipids. Multiple receptor and nonreceptor mediated pathways function in macrophage uptake of TRL. TRL also induce expression of adhesion molecules, cyclooxygenase-2 and heme-oxygenase-1 in endothelial cells, and activate intracellular signaling pathways involving mitogen-activated protein kinases, NE-kappa B and Nrf2. Many of these effects are strongly influenced by dietary components carried in TRL. There is extensive evidence indicating that raised postprandial TRL levels are a risk factor for atherosclerosis, but the molecular mechanisms involved are only now becoming appreciated. Here, we review current understanding of the mechanisms by which TRL influence vascular cell function. (C) 2013 Elsevier Ltd. All rights reserved.
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