Linked Life Data

17999635

Source:http://linkedlifedata.com/resource/pubmed/id/17999635

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-12-26
pubmed:abstractText
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive disorder in which excessive deposition of extracellular matrix leads to irreversible scarring of interstitial lung tissue. The etiology of IPF remains unknown, but growing evidence suggests that disequilibrium in oxidant/antioxidant balance contributes significantly. IPF is currently regarded as a fibroproliferative disorder triggered by repeated alveolar epithelial cell injury. Oxidative stress plays a role in many processes involved in alveolar epithelial cell injury and fibrogenesis. Here we review the role of oxidative stress in IPF, and other forms of pulmonary fibrosis, with particular attention to antioxidant defenses regulated by the redox-sensitive transcription factor nuclear factor, erythroid derived 2, like (Nrf2). Nrf2 binds specific antioxidant response elements (AREs) in the promoter of antioxidant enzyme and defense protein genes and regulates their expression in many tissue types. Nrf2 protects from several phenotypes in which enhanced oxidative burden contributes to disease pathogenesis, including cancer, acute lung injury, and pulmonary fibrosis. We suggest that promoter polymorphisms in human NRF2 may contribute to IPF susceptibility, although this hypothesis has not been tested. Pulmonary fibrosis is a highly complex disease and involves multiple genes and processes, and new therapies for cellular and molecular targets involved in pathogenic mechanisms are needed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1523-0864
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
321-32
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Oxidative stress and antioxidants in the pathogenesis of pulmonary fibrosis: a potential role for Nrf2.
pubmed:affiliation
Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA.
pubmed:publicationType
Journal Article, Review