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Thioredoxin Reductase 1
Thioredoxin-related mechanisms in hyperoxic lung injury in mice.
Aurothioglucose does not improve alveolarization or elicit sustained Nrf2 activation in C57BL/6 models of bronchopulmonary dysplasia.
Antioxidants & bronchopulmonary dysplasia: Beating the system or beating a dead horse?
Thioredoxin Reductase-1 Inhibition Augments Endogenous Glutathione-Dependent Antioxidant Responses in Experimental Bronchopulmonary Dysplasia.
Thioredoxin-interacting protein inhibits hypoxia-inducible factor transcriptional activity.
Thioredoxin-1 mediates hypoxia-induced pulmonary artery smooth muscle cell proliferation.
The thioredoxin reductase-1 inhibitor aurothioglucose attenuates lung injury and improves survival in a murine model of acute respiratory distress syndrome.
The thioredoxin reductase inhibitor auranofin induces heme oxygenase-1 in lung epithelial cells via Nrf2-dependent mechanisms.
Alterations of the thioredoxin system by hyperoxia: implications for alveolar development.
Thioredoxin reductase inhibition elicits Nrf2-mediated responses in Clara cells: implications for oxidant-induced lung injury.
The thioredoxin system in neonatal lung disease.
Thioredoxin Reductase Inhibition Attenuates Neonatal Hyperoxic Lung Injury and Enhances Nuclear Factor E2-Related Factor 2 Activation.
Selenium supplementation of lung epithelial cells enhances nuclear factor E2-related factor 2 (Nrf2) activation following thioredoxin reductase inhibition.
Selenium-independent antioxidant and anti-inflammatory effects of thioredoxin reductase inhibition in alveolar macrophages.