Disruption of Nrf2 impairs the resolution of hyperoxia-induced acute lung injury and inflammation in mice.

ABSTRACT: Aberrant tissue repair and persistent inflammation following oxidant-mediated acute lung injury (ALI) can lead to the development and progression of various pulmonary diseases, but the mechanisms underlying these processes remain unclear. Hyperoxia is widely used in the treatment of pulmonary diseases, but the effects of this oxidant exposure in patients undergoing recovery from ALI are not clearly understood. Nrf2 has emerged as a crucial transcription factor that regulates oxidant stress through the induction of several detoxifying enzymes and other proteins. Using an experimental model of hyperoxia-induced ALI, we have examined the role of oxidant stress in resolving lung injury and inflammation. We found that when exposed to sublethal (72 h) hyperoxia, Nrf2-deficient, but not wild-type

SUBMITTER: Reddy NM 

PROVIDER: S-EPMC2820248 | biostudies-literature | 2009 Jun

REPOSITORIES: biostudies-literature