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Cyclooxygenase-2 in newborn hyperoxic lung injury.
Maternal dietary docosahexaenoic acid supplementation attenuates fetal growth restriction and enhances pulmonary function in a newborn mouse model of perinatal inflammation.
miR-29b supplementation decreases expression of matrix proteins and improves alveolarization in mice exposed to maternal inflammation and neonatal hyperoxia.
Aurothioglucose does not improve alveolarization or elicit sustained Nrf2 activation in C57BL/6 models of bronchopulmonary dysplasia.
Maternal docosahexaenoic acid supplementation decreases lung inflammation in hyperoxia-exposed newborn mice.
Thioredoxin Reductase-1 Inhibition Augments Endogenous Glutathione-Dependent Antioxidant Responses in Experimental Bronchopulmonary Dysplasia.
Club Cell Heme Oxygenase-1 Deletion: Effects in Hyperoxia-Exposed Adult Mice.
Thioredoxin-interacting protein inhibits hypoxia-inducible factor transcriptional activity.
Alterations in VASP phosphorylation and profilin1 and cofilin1 expression in hyperoxic lung injury and BPD.
Differential responses in the lungs of newborn mouse pups exposed to 85% or >95% oxygen.
Alterations of the thioredoxin system by hyperoxia: implications for alveolar development.
Hyperoxia exposure alters hepatic eicosanoid metabolism in newborn mice.
The thioredoxin system in neonatal lung disease.
Thioredoxin Reductase Inhibition Attenuates Neonatal Hyperoxic Lung Injury and Enhances Nuclear Factor E2-Related Factor 2 Activation.
Aurothioglucose enhances proangiogenic pathway activation in lungs from room air and hyperoxia-exposed newborn mice.
Glutathione reductase deficiency alters lung development and hyperoxic responses in neonatal mice.
MicroRNA 219-5p inhibits alveolarization by reducing platelet derived growth factor receptor-alpha.
Microbial-induced Redox Imbalance in the Neonatal Lung Is Ameliorated by Live Biotherapeutics.