ArticleRadiation and environmental biophysics2019
The ion channel, TRPM2, contributes to the pathogenesis of radiodermatitis.
Article in Radiation and environmental biophysics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 6 citations in OpenAlex.
- Macrophage derived VEGF regulates macrophage senescence to inhibit radiation-induced dermatitis.Journal of translational medicine · 2025Article
- Combinatorial Therapy of Cancer: Possible Advantages of Involving Modulators of Ionic Mechanisms.Cancers · 2022Review
- Radiation-induced lung toxicity - cellular and molecular mechanisms of pathogenesis, management, and literature review.Radiation oncology (London, England) · 2020Review
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
Radiodermatitis is a painful side effect for cancer patients undergoing radiotherapy. Irradiation of the skin causes inflammation and breakdown of the epidermis and can lead to significant morbidity and mortality in severe cases, as seen in exposure from accidents or weapons such as "dirty bombs" and ultimately leads to tissue fibrosis. However, the pathogenesis of radiodermatitis is not fully understood. Using a mouse model of radiodermatitis, we showed that the Transient Receptor Potential Melastatin 2 (TRPM2) ion channel plays a significant role in the development of dermatitis following exposure to ionizing radiation. Irradiated TRPM2-deficient mice developed less inflammation, fewer severe skin lesions and decreased fibrosis when compared to wild type mice. The TRPM2-deficient mice also showed a faster recovery period as seen by their increased weight gain post irradiation. Finally, TRPM2-deficient mice exhibited lower systemic inflammation with a reduction in inflammatory cytokines present in the serum. These findings suggest that TRPM2 may be a potential therapeutic target for reducing the severity of radiodermatitis.
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Registered trials
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