Abstract
The role of oxidative stress in regulating transcription factors and specific gene responses in critical illness is a new and emerging area. A better understanding of the proinflammatory oxidant stimuli of reactive oxygen species generation and how this generates the clinical phenotype of acute lung injury by regulating gene expression may allow the development of new therapeutic strategies. In his review John Haddad describes the present data and role for transcription factors nuclear factor-κB and hypoxia-inducible factor-1α in acute lung injury.
MeSH terms
-
DNA-Binding Proteins / genetics
-
DNA-Binding Proteins / metabolism*
-
Humans
-
Hypoxia-Inducible Factor 1
-
Hypoxia-Inducible Factor 1, alpha Subunit
-
NF-kappa B / genetics
-
NF-kappa B / metabolism*
-
Nuclear Proteins / genetics
-
Nuclear Proteins / metabolism*
-
Oxidative Stress
-
Respiratory Distress Syndrome / genetics
-
Respiratory Distress Syndrome / metabolism*
-
Transcription Factors / genetics
-
Transcription Factors / metabolism*
-
Up-Regulation
Substances
-
DNA-Binding Proteins
-
HIF1A protein, human
-
Hypoxia-Inducible Factor 1
-
Hypoxia-Inducible Factor 1, alpha Subunit
-
NF-kappa B
-
Nuclear Proteins
-
Transcription Factors