ArticleOxidative medicine and cellular longevity2018
Thioredoxin-1 Protects Bone Marrow-Derived Mesenchymal Stromal Cells from Hyperoxia-Induced Injury In Vitro.
Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Punicalagin alleviates senile osteoporosis by inhibiting the senescence of bone mesenchymal stem cells via NRF2/HO-1 pathway.Regenerative therapy · 2026Article
- Multi-omics integration and machine learning identify a novel gene signature consisting of CCDC141, CHI3L2, RIMKLB, and PDLIM7 in bronchopulmonary dysplasia associated with neutrophil-driven immune dysregulation.Clinics (Sao Paulo, Brazil) · 2026Article
- Enhancing osteogenic differentiation of diabetic tendon stem/progenitor cells through hyperoxia: Unveiling ROS/HIF-1α signalling axis.Journal of cellular and molecular medicine · 2024Article
- Post-translational modifications and bronchopulmonary dysplasia.Frontiers in pediatrics · 2024Review
- Effects of Antioxidants in Human Milk on Bronchopulmonary Dysplasia Prevention and Treatment: A Review.Frontiers in nutrition · 2022Review
- Edaravone prevents high glucose-induced injury in retinal Müller cells through thioredoxin1 and the PGC-1α/NRF1/TFAM pathway.Pharmaceutical biology · 2021Article
- An NRF2 Perspective on Stem Cells and Ageing.Frontiers in aging · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe poor survival rate of mesenchymal stromal cells (MSC) transplanted into recipient lungs greatly limits their therapeutic efficacy for diseases like bronchopulmonary dysplasia (BPD). The aim of this study is to evaluate the effect of thioredoxin-1 (Trx-1) overexpression on improving the potential for bone marrow-derived mesenchymal stromal cells (BMSCs) to confer resistance against hyperoxia-induced cell injury.
methods80% O
resultTrx-1 overexpression significantly reduced hyperoxia-induced BMSC apoptosis and increased cell proliferation. We demonstrated that Trx-1 overexpression upregulated the levels of superoxide dismutase and glutathione peroxidase as well as downregulated the production of ROS. Furthermore, we illustrated that Trx-1 protected BMSCs against hyperoxic injury via decreasing the ASK1/P38 MAPK activation rate.
conclusionThese results demonstrate that Trx-1 overexpression improved the ability of BMSCs to counteract hyperoxia-induced injury, thus increasing their potential to treat hyperoxia-induced lung diseases such as BPD.
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Registered trials
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