The transcription factor NRF2 protects against pulmonary fibrosis HYE-YOUN CHO * ,† ,1 , SEKHAR P. M. REDDY * , MASAYUKI YAMAMOTO ‡ and STEVEN R. KLEEBERGER * ,† * Department of Environmental Health Sciences, The Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA; † Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA; and ‡ Institute of Basic Medical Sciences and Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tennoudai, Tsukuba, Japan 1 Correspondence: Laboratory of Respiratory Biology, NIEHS, NIH, Research Triangle Park, North Carolina 27709, USA. E-mail: cho2@niehs.nih.gov <h3>SPECIFIC AIMS</h3> Molecular mechanisms of fibrosis are poorly understood, although reactive oxygen species (ROS) are thought to have an important role. The primary objective of this study was to determine whether NF-E2-related factor 2 (NRF2), a key transcriptional regulator for antioxidant response element (ARE) -mediated induction of cellular antioxidants and detoxifying proteins, protects against pathogenesis of pulmonary fibrosis. To test this hypothesis, we exposed mice with targeted deletion of Nrf2 (ICR/Sv129- Nrf2 –/– ) and wild-type (ICR/Sv129- Nrf2 +/+ ) mice to bleomycin and compared pulmonary injury and fibrotic responses. <h3>PRINCIPAL FINDINGS</h3> 1.
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