Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2005-4-11
pubmed:abstractText
Endothelial cell dysfunction is emerging as an ultimate culprit for diverse cardiovascular diseases and cardiovascular complications of chronic renal diseases, yet the definition of this new syndrome, its pathophysiology, and therapy remain poorly defined. Here, I summarize some molecular mechanisms leading from hyperhomocystinemia, elevated asymmetric dimethylarginine, and advanced glycolation end product-modified protein level to the proatherogenic, prothrombogenic, and proinflammatory endothelial phenotype and offer a model of endothelial dysfunction based on the interconnectedness of diverse functions. Finally, several therapeutic strategies to prevent and correct endothelial dysfunction are discussed in the light of uncertainty of their action modulated by the endothelial dysfunction per se.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1931-857X
pubmed:author
pubmed:issnType
Print
pubmed:volume
288
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F871-80
pubmed:dateRevised
2011-4-28
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Endothelial cell dysfunction: can't live with it, how to live without it.
pubmed:affiliation
Department of Nephrology and Renal Research Institute, Department of Medicine, New York Medical College, Valhalla, New York 10595, USA. Michael_Goligorsky@nymc.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't