ReviewAntioxidants & redox signaling2014
The thioredoxin system in neonatal lung disease.
Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Redox Regulation of KAntioxidants & redox signaling · 2024Review
- Microbial-induced Redox Imbalance in the Neonatal Lung Is Ameliorated by Live Biotherapeutics.American journal of respiratory cell and molecular biology · 2023Article
- Effects of Antioxidants in Human Milk on Bronchopulmonary Dysplasia Prevention and Treatment: A Review.Frontiers in nutrition · 2022Review
- Tempol differently affects cellular redox changes and antioxidant enzymes in various lung-related cells.Scientific reports · 2021Article
- Hydrogen Sulfide-Clues from Evolution and Implication for Neonatal Respiratory Diseases.Children (Basel, Switzerland) · 2021Review
- Selenium-independent antioxidant and anti-inflammatory effects of thioredoxin reductase inhibition in alveolar macrophages.Life sciences · 2020Article
- Thioredoxin Reductase-1 Inhibition Augments Endogenous Glutathione-Dependent Antioxidant Responses in Experimental Bronchopulmonary Dysplasia.Oxidative medicine and cellular longevity · 2019Article
- Selenium supplementation of lung epithelial cells enhances nuclear factor E2-related factor 2 (Nrf2) activation following thioredoxin reductase inhibition.Redox biology · 2018Article
- The thioredoxin reductase inhibitor auranofin induces heme oxygenase-1 in lung epithelial cells via Nrf2-dependent mechanisms.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Aurothioglucose does not improve alveolarization or elicit sustained Nrf2 activation in C57BL/6 models of bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- A novel mouse model for the identification of thioredoxin-1 protein interactions.Free radical biology & medicine · 2016Article
- Neonatal lung function and therapeutics.Antioxidants & redox signaling · 2014Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
significanceFetal lung development takes place in hypoxia meaning that premature birth is hyperoxia for the prematurely born infant. The most common respiratory morbidity afflicting premature infants is bronchopulmonary dysplasia (BPD). Pathophysiologically, BPD represents the impact of injury, including O2 toxicity, to the immature developing lung that causes arrested lung development. RECENT ADVANCES: The thioredoxin (Trx) system, which is predominantly expressed in pulmonary epithelia in the newborn lung, acts as an antioxidant system; however, it is increasingly recognized as a key redox regulator of signal transduction and gene expression via thiol-disulfide exchange reactions. CRITICAL ISSUES: This review focuses on the contribution of Trx family proteins toward normal and aberrant lung development, in particular, the roles of the Trx system in hyperoxic responses of alveolar epithelial cells, aberrant lung development in animal models of BPD, O2-dependent signaling processes, and possible therapeutic efficacy in preventing O2-mediated lung injury. FUTURE DIRECTIONS: The significant contribution of the Trx system toward redox regulation of key developmental pathways necessary for proper lung development suggests that therapeutic strategies focused on preserving pulmonary Trx function could significantly improve the outcomes of prematurely born human infants.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.