Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11-12
pubmed:dateCreated
2006-5-22
pubmed:abstractText
Reactive oxygen species (ROS) play important roles in the pathogenesis of cardiovascular disease. Surprisingly, large clinical trials have shown that ROS scavenging by antioxidant vitamins is ineffective or harmful. Therefore, prevention of ROS formation, by targeting specific sources of superoxide anion and other ROS, might prove beneficial. Potential targets include the NADPH oxidases (Nox enzymes), xanthine oxidase, endothelial nitric oxide synthase and mitochondrial oxidases. Nox enzymes play a central role because they can regulate other enzymatic sources of ROS. Statins, angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists block upstream signaling of Nox activation, which contributes to their clinical effectiveness. Here, we discuss novel possibilities where drugs that directly inhibit Nox activation could successfully inhibit oxidative stress.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1359-6446
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
524-33
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Vascular NADPH oxidases as drug targets for novel antioxidant strategies.
pubmed:affiliation
Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA. tguzik@emory.edu
pubmed:publicationType
Journal Article, Review