Linked Life Data

19485918

Source:http://linkedlifedata.com/resource/pubmed/id/19485918

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-5-28
pubmed:abstractText
Atherosclerotic plaque destabilization is a major cause of unstable angina, myocardial infarction, and sudden cardiac death. Macrophages, which are an essential component of unstable plaques, play a pivotal role in the destabilization process, whereas smooth muscle cells contribute to plaque stability. Selective removal of macrophages is therefore an interesting pharmacological objective to stabilize vulnerable, rupture-prone lesions. Pharmacological agents such as clodronate, nitric oxide donors, mammalian target of rapamycin (mTOR) inhibitors, protein synthesis inhibitors, and statins, that are capable of selectively depleting macrophages in atherosclerotic plaques without affecting smooth muscle or endothelial cells, have recently been identified. This review focuses on the mechanism of action of these drugs as well as on the potential pitfalls of drug-induced macrophage depletion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1875-6212
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
495-508
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Selective removal of macrophages in atherosclerotic plaques as a pharmacological approach for plaque stabilization: benefits versus potential complications.
pubmed:affiliation
Division of Pharmacology, University of Antwerp, Antwerp, Belgium. valerie.croons@ua.ac.be
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't