Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2007-8-6
pubmed:abstractText
In response to various stimuli, membrane lipid rafts (LRs) are clustered to aggregate or recruit NADPH oxidase subunits and related proteins in vascular endothelial cells (ECs), forming redox signaling platforms. These LR signaling platforms may play important roles in the normal regulation of endothelial function and in the development of endothelial dysfunction or injury under pathological conditions. This LR-mediated mechanism now takes center stage in cell signaling for the regulation of many cellular activities or cell function such as ECs redox signaling, phagosomal activity of phagocytes, and cell apopotosis of lymphocytes. This brief review summarizes current evidence that relates to the formation of LR redox signaling platforms and their features in ECs, the functional significance of these signaling platforms in mediating death receptor activation-induced endothelial dysfunction, and the mechanisms initiating or promoting the formation of these platforms. It is expected that information provided here will help readers to understand this new signaling mechanism and perhaps extend the LR signaling platform concept to other research areas related to death receptors, redox signaling, endothelial biology, and cell/molecular biology of the cardiovascular system.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1523-0864
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1457-70
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Lipid raft redox signaling platforms in endothelial dysfunction.
pubmed:affiliation
Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA.
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural