Linked Life Data

16877880

Source:http://linkedlifedata.com/resource/pubmed/id/16877880

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
2006-7-31
pubmed:abstractText
Plasma levels of lipoprotein(a), Lp(a), is an independent risk factor for cardiovascular disease. Lp(a) has many properties in common with low-density lipoprotein (LDL), including a cholesteryl ester-rich lipid core and the presence of one copy of apolipoprotein B-100; both apoB-100 and the lipid core are pro-atherogenic. In addition, Lp(a) contains a unique hydrophilic, carbohydrate-rich protein, apo(a), linked to apoB through a single disulfide bond connecting the C-terminal regions of the two proteins. The similarities between apolipoprotein(a), apo(a), and plasminogen has initiated numerous studies on the possible role of Lp(a) as a prothrombotic agent. Studies to date suggest that Lp(a) has antifibrinolytic and procoagulant properties. In this review, we summarize recent studies focused on the interaction between Lp(a) and platelets. Collectively, results to date illustrate that thrombogenicity associated with Lp(a) could be due to risk associated with the LDL moiety, with the apo(a) moiety, or from the combination of those in Lp(a). Present findings suggest that the various components of Lp(a) may impact to a varying degree on different underlying pathways involved in platelet activation and aggregation. On balance, results indicate an effect by Lp(a) on platelet function and future studies focused on specific Lp(a) components, such as the role of apo(a) and of the LDL-like lipid moiety, are needed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1424-8832
pubmed:author
pubmed:copyrightInfo
Copyright 2006 S. Karger AG, Basel.
pubmed:issnType
Print
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
314-21
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Lipoprotein(a) and thrombocytes: potential mechanisms underlying cardiovascular risk.
pubmed:affiliation
Department of Medicine, University of California Davis, 95817, USA.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't