Regulation of hyperoxia-induced neonatal lung injury via post-translational cysteine redox modifications.

ABSTRACT: Preterm infants and patients with lung disease often have excess fluid in the lungs and are frequently treated with oxygen, however long-term exposure to hyperoxia results in irreversible lung injury. Although the adverse effects of hyperoxia are mediated by reactive oxygen species, the full extent of the impact of hyperoxia on redox-dependent regulation in the lung is unclear. In this study, neonatal mice overexpressing the beta-subunit of the epithelial sodium channel (β-ENaC) encoded by Scnn1b and their wild type (WT; C57Bl6) littermates were utilized to study the pathogenesis of high fraction inspired oxygen (FiO₂)-induced lung injury. Results showed that O₂-induced lung injury in transgenic Scnn1b mice is attenuated following chronic O₂ exposure. To te

SUBMITTER: Zhang T 

PROVIDER: S-EPMC9307955 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature