ArticleToxicological sciences : an official journal of the Society of Toxicology2015
Radiation-induced lung injury and inflammation in mice: role of inducible nitric oxide synthase and surfactant protein D.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Serum surfactant protein D as a significant biomarker for predicting occurrence, progression, acute exacerbation, and mortality in interstitial lung disease: a systematic review and meta-analysis.Frontiers in immunology · 2025Pooled it
- Targeting Oxidative and Nitrosative Stress: Mechanistic Insights and Therapeutic Strategies for Radiation-Induced Lung Injury.Journal of inflammation research · 2026Review
- Serum amyloid A contributes to radiation-induced lung injury by activating macrophages through FPR2/Rac1/NF-κB pathway.International journal of biological sciences · 2024Article
- Targeting Tumor Necrosis Factor Alpha to Mitigate Lung Injury Induced by Mustard Vesicants and Radiation.Disaster medicine and public health preparedness · 2023Review
- Discovery of the radio-protecting effect of Ecliptae Herba, its constituents and targeting p53-mediated apoptosisActa pharmaceutica Sinica. B · 2023Article
- Lung injury and oxidative stress induced by inhaled chlorine in mice is associated with proinflammatory activation of macrophages and altered bioenergetics.Toxicology and applied pharmacology · 2023Article
- Microarray analysis of hub genes, non-coding RNAs and pathways in lung after whole body irradiation in a mouse model.International journal of radiation biology · 2023Article
- The roles of CC chemokines in response to radiation.Radiation oncology (London, England) · 2022Review
- Lung Pneumonitis and Fibrosis in Cancer Therapy: A Review on Cellular and Molecular Mechanisms.Current drug targets · 2022Review
- Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques.Journal of inflammation research · 2022Review
- [Research progress on macrophage in radiation induced lung injury].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Review
- Ginkgo biloba Extract EGb761 Attenuates Bleomycin-Induced Experimental Pulmonary Fibrosis in Mice by Regulating the Balance of M1/M2 Macrophages and Nuclear Factor Kappa B (NF-κB)-Mediated Cellular Apoptosis.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Modeling radiation-induced lung injury: lessons learned from whole thorax irradiation.International journal of radiation biology · 2020Review
- Promising role of filgrastim and α-tocopherol succinate in amelioration of gastrointestinal acute radiation syndrome (GI-ARS) in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2019Article
- Mitigation of Radiation-Induced Lung Pneumonitis and Fibrosis Using Metformin and Melatonin: A Histopathological Study.Medicina (Kaunas, Lithuania) · 2019Article
- Role of Macrophages in Acute Lung Injury and Chronic Fibrosis Induced by Pulmonary Toxicants.Toxicological sciences : an official journal of the Society of Toxicology · 2019Review
- Radiation-Induced Normal Tissue Damage: Oxidative Stress and Epigenetic Mechanisms.Oxidative medicine and cellular longevity · 2019Review
- A Potential Biomarker for Predicting the Risk of Radiation-Induced Fibrosis in the Lung.Radiation research · 2018Article
- Protective Role of Surfactant Protein-D Against Lung Injury and Oxidative Stress Induced by Nitrogen Mustard.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Reduction-oxidation (redox) system in radiation-induced normal tissue injury: molecular mechanisms and implications in radiation therapeutics.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Reactive nitrogen species (RNS) generated after exposure to radiation have been implicated in lung injury. Surfactant protein D (SP-D) is a pulmonary collectin that suppresses inducible nitric oxide synthase (iNOS)-mediated RNS production. Herein, we analyzed the role of iNOS and SP-D in radiation-induced lung injury. Exposure of wild-type (WT) mice to γ-radiation (8 Gy) caused acute lung injury and inflammation, as measured by increases in bronchoalveolar lavage (BAL) protein and cell content at 24 h. Radiation also caused alterations in SP-D structure at 24 h and 4 weeks post exposure. These responses were blunted in iNOS(-/-) mice. Conversely, loss of iNOS had no effect on radiation-induced expression of phospho-H2A.X or tumor necrosis factor (TNF)-α. Additionally, at 24 h post radiation, cyclooxygenase expression and BAL lipocalin-2 levels were increased in iNOS(-/-) mice, and heme oxygenase (HO)-1(+) and Ym1(+) macrophages were evident. Loss of SP-D resulted in increased numbers of enlarged HO-1(+) macrophages in the lung following radiation, along with upregulation of TNF-α, CCL2, and CXCL2, whereas expression of phospho-H2A.X was diminished. To determine if RNS play a role in the altered sensitivity of SP-D(-/-) mice to radiation, iNOS(-/-)/SP-D(-/-) mice were used. Radiation-induced injury, oxidative stress, and tissue repair were generally similar in iNOS(-/-)/SP-D(-/-) and SP-D(-/-) mice. In contrast, TNF-α, CCL2, and CXCL2 expression was attenuated. These data indicate that although iNOS is involved in radiation-induced injury and altered SP-D structure, in the absence of SP-D, it functions to promote proinflammatory signaling. Thus, multiple inflammatory pathways contribute to the pathogenic response to radiation.
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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.