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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2003-10-31
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pubmed:abstractText |
Reactive oxygen species generated from NADPH oxidase(s) in airway smooth muscle cells and pulmonary artery smooth muscle cells are important signaling intermediates. Nox4 appears to be the predominant gp91 homologue in these cells. However, expression of NADPH oxidase components is dependent on phenotype, and different homologues may be expressed during different functional states of the cell. NADPH oxidase(s) appear to be important not only for mitogenesis by these cells, but also for O(2) sensing. The regulation of NADPH oxidase(s) in airway and pulmonary artery smooth muscle cells has important implications for the pathobiochemistry of asthma and pulmonary vascular diseases.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1523-0864
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
751-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:14588148-Animals,
pubmed-meshheading:14588148-Cell Division,
pubmed-meshheading:14588148-Humans,
pubmed-meshheading:14588148-Membrane Glycoproteins,
pubmed-meshheading:14588148-Models, Chemical,
pubmed-meshheading:14588148-Muscle, Smooth, Vascular,
pubmed-meshheading:14588148-Myocytes, Smooth Muscle,
pubmed-meshheading:14588148-NADPH Oxidase,
pubmed-meshheading:14588148-Oxygen,
pubmed-meshheading:14588148-Phenotype,
pubmed-meshheading:14588148-Reactive Oxygen Species,
pubmed-meshheading:14588148-Signal Transduction
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pubmed:year |
2003
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pubmed:articleTitle |
The role of endogenous NADPH oxidases in airway and pulmonary vascular smooth muscle function.
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pubmed:affiliation |
Department of Internal Medicine, University of Utah School of Medicine, Medical Service, Salt Lake City, UT, USA. john.hoidal@hsc.utah.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review,
Research Support, Non-U.S. Gov't
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