Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2005-8-15
pubmed:abstractText
High-density lipoprotein (HDL) appears to have evolved as part of the innate immune system, which in part uses an enhanced oxidative state as a nonspecific means of protecting against many pathogens. In the absence of acute or chronic inflammation, HDL is anti-inflammatory in mice, rabbits, and humans. However, with the onset of a systemic inflammatory state such as what occurs in atherosclerosis, HDL becomes pro-inflammatory, enhancing the inflammatory response. The major apolipoprotein of HDL is apoA-I, which may be altered by oxidative processes in patients with atherosclerosis. As a result, HDL from such patients is less efficient in promoting cellular cholesterol efflux. The ability of HDL to inhibit the inflammatory properties of oxidized phospholipids and low-density lipoproteins is also significantly altered. In mice and monkeys, the administration of an apoA-I-mimetic peptide renders pro-inflammatory HDL anti-inflammatory, improves HDL-mediated cellular cholesterol efflux; in mice, it dramatically inhibits atherosclerosis. Understanding the role of HDL in inflammation may lead to new diagnostic and therapeutic approaches to atherosclerosis and other inflammatory conditions.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1050-1738
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
158-61
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
The role of high-density lipoprotein in inflammation.
pubmed:affiliation
Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California in Los Angeles, Room 47-123 CHS, 10833 Le Conte Avenue, Los Angeles, CA 90095-1679, USA. mnavab@mednet.ucla.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural