ArticleInternational journal of molecular sciences2021
Metformin Protects against Radiation-Induced Acute Effects by Limiting Senescence of Bronchial-Epithelial Cells.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Effects of Fractionated Low Dose Ionizing Radiation on Cellular Senescence in Mouse Lung Tissue.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Unraveling the molecular landscape of chronic radiation injury: From oxidative stress signaling to translational modeling (Review).International journal of molecular medicine · 2026Review
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Ionizing radiation promotes lung injury by inducing ferroptosis-driven senescence in epithelial cells via NCOA4-mediated ferritinophagy.Redox biology · 2026Article
- Molecular mechanisms and network interactions in radiation-induced lung injury.Frontiers in physiology · 2026Review
- Senescent fibroblasts modulate the radiation response of neighboring epithelial cells.Cell death discovery · 2025Article
- Analysis of factors influencing lung cancer in patients with type 2 diabetes mellitus.Medicine · 2025Observational
- Preventive Effect of Metformin in Radiation-Induced Xerostomia.Advanced biology · 2025Article
- The vascular endothelium as decision maker in lung injury.Frontiers in cell and developmental biology · 2025Review
- Matrix-free human lung organoids derived from induced pluripotent stem cells to model lung injury.Stem cell research & therapy · 2024Article
- Addition of Polyphenols to Drugs: The Potential of Controlling "Inflammaging" and Fibrosis in Human Senescent Lung Fibroblasts In Vitro.International journal of molecular sciences · 2024Article
- Review
- Glycyrrhizin alleviates radiation-induced lung injury by regulating the NLRP3 inflammasome through endoplasmic reticulum stress.Toxicology research · 2024Article
- Non-small cell lung cancer cells and concomitant cancer therapy induce a resistance-promoting phenotype of tumor-associated mesenchymal stem cells.Frontiers in oncology · 2024Article
- Cellular Senescence and Frailty in Transplantation.Current transplantation reports · 2023Article
- Considerations of Medical Preparedness to Assess and Treat Various Populations During a Radiation Public Health Emergency.Radiation research · 2023Review
- Metformin mitigates SASP secretion and LPS-triggered hyper-inflammation in Doxorubicin-induced senescent endothelial cells.Frontiers in aging · 2023Article
- Senescence and the tumor-immune landscape: Implications for cancer immunotherapy.Seminars in cancer biology · 2022Review
- Cellular senescence and senolytics: the path to the clinic.Nature medicine · 2022Review
- Senotherapy Protects against Cisplatin-Induced Ovarian Injury by Removing Senescent Cells and Alleviating DNA Damage.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Radiation-induced damage to normal lung parenchyma remains a dose-limiting factor in thorax-associated radiotherapy (RT). Severe early and late complications with lungs can increase the risk of morbidity in cancer patients after RT. Herein, senescence of lung epithelial cells following RT-induced cellular stress, or more precisely the respective altered secretory profile, the senescence-associated secretory phenotype (SASP), was suggested as a central process for the initiation and progression of pneumonitis and pulmonary fibrosis. We previously reported that abrogation of certain aspects of the secretome of senescent lung cells, in particular, signaling inhibition of the SASP-factor Ccl2/Mcp1 mediated radioprotection especially by limiting endothelial dysfunction. Here, we investigated the therapeutic potential of a combined metformin treatment to protect normal lung tissue from RT-induced senescence and associated lung injury using a preclinical mouse model of radiation-induced pneumopathy. Metformin treatment efficiently limited RT-induced senescence and SASP expression levels, thereby limiting vascular dysfunctions, namely increased vascular permeability associated with increased extravasation of circulating immune and tumor cells early after irradiation (acute effects). Complementary in vitro studies using normal lung epithelial cell lines confirmed the senescence-limiting effect of metformin following RT finally resulting in radioprotection, while fostering RT-induced cellular stress of cultured malignant epithelial cells accounting for radiosensitization. The radioprotective action of metformin for normal lung tissue without simultaneous protection or preferable radiosensitization of tumor tissue might increase tumor control probabilities and survival because higher radiation doses could be used.
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Registered trials
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