ArticleJCI insight2026
A human ex vivo model of radiation-induced skin injury recapitulates p53-driven profibrotic response to radiotherapy.
Article in JCI insight, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Epithelial-mesenchymal transition in cutaneous fibrosis disease: from mechanisms to therapy.Frontiers in immunology · 2026Review
Corrections and comments
- Update ofA human2025
Authors and funding
11 authors.
Funding
Abstract
Cutaneous radiation injury is an unintended consequence of radiotherapy for many common cancers and can progress to debilitating radiation-induced skin fibrosis (RISF). Existing radiation injury models do not fully capture the skin toxicities observed in patients, contributing to the lack of efficacious therapies to mitigate RISF. To address this, we developed an ex vivo human skin model that recapitulates the temporal radiation injury and RISF response. Human skin explants (n = 12) subjected to ionizing radiation demonstrated DNA double-stranded breaks and robust p53-driven transcriptional programming of cell cycle arrest, apoptosis, and senescence compared with nonirradiated controls. Irradiated skin also exhibited induction of pro-inflammatory cytokines, epithelial-mesenchymal transition, profibrotic TGF-β1-mediated signaling, and thickened collagen over time. P53 regulators murine double minute 2 (MDM2) and miR-34a were induced after irradiation and may be leveraged to modulate injury response. Notably, RNA-sequencing of postradiotherapy breast skin from patients who had undergone mastectomy showed similar p53, inflammatory, and TGF-β1 signatures as the ex vivo model, supporting its translational relevance. Together, this model provides a platform for identifying biomarkers and testing therapies to prevent or mitigate cutaneous radiation toxicities. Targeting the dynamic p53-driven profibrotic radiation response represents a potentially new therapeutic avenue to improve quality of life for patients after radiotherapy.
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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.