ArticleOxidative medicine and cellular longevity2019
CD28 Deficiency Ameliorates Blast Exposure-Induced Lung Inflammation, Oxidative Stress, Apoptosis, and T Cell Accumulation in the Lungs via the PI3K/Akt/FoxO1 Signaling Pathway.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 34 citations in OpenAlex.
- Establishment and evaluation of anFrontiers in public health · 2022Trial
- Research progress on biomarkers of blast lung injury: Transition from traditional indicators to novel molecular markers.iScience · 2026Review
- Research progress on resistance mechanisms to CAR-T cell therapy in diffuse large B-cell lymphoma.Frontiers in oncology · 2026Review
- Integrated bioinformatics analysis unravels mitochondrial-immune crosstalk and infiltration dynamics in sepsis progression.European journal of medical research · 2025Article
- Review
- Article
- Characteristics of inflammatory response and repair after experimental blast lung injury in rats.PloS one · 2023Article
- Exosomes: Potential Player in Endothelial Dysfunction in Cardiovascular Disease.Cardiovascular toxicology · 2022Review
- FOXO1 Is a Critical Switch Molecule for Autophagy and Apoptosis of Sow Endometrial Epithelial Cells Caused by Oxidative Stress.Oxidative medicine and cellular longevity · 2021Article
- rhKGF-2 Attenuates Smoke Inhalation Lung Injury of RatsFrontiers in pharmacology · 2021Article
- Potential Functions of the tRNA-Derived Fragment tRF-Gly-GCC Associated With Oxidative Stress in Radiation-Induced Lung Injury.Dose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although CD28 is associated with the expression of inflammatory mediators, apoptosis-related protein, immunosuppression, and tumorigenesis, the effects of CD28 deficiency on blast exposure-induced lung injury have not been investigated. In this study, we have explored the effects of CD28 on blast exposure-induced lung injury and studied its potential molecular mechanisms. A mouse model of blast exposure-induced acute lung injury was established. Sixty C57BL/6 wild-type (WT) and CD28 knockout (CD28
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