Evidence map›Paper›PMID 41764525›Full record

ArticleRadiation oncology (London, England)2026

Preliminary mechanistic study of mitochondrial function in intestinal protection mediated by high-energy X-ray FLASH radiotherapy.

Xiaofei Hao, Huan Du, Binwei Lin, Decai Wang, Wei Wu, Mingming Tang, Huayan Zhang, Yihan Zhu, Yu Zhang, Yiwei Yang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Radiation oncology (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Reduced corneal toxicity following whole brain irradiation in mice.Clinical and translational radiation oncology · 2026
    Article
  2. Article
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Xiaofei HaoSchool of Medicine, Mianyang Central Hospital, University of Electronic Science and Technology of China, Mianyang, 621000, China.
Huan DuSchool of Medicine, Mianyang Central Hospital, University of Electronic Science and Technology of China, Mianyang, 621000, China.
Binwei LinSchool of Medicine, Mianyang Central Hospital, University of Electronic Science and Technology of China, Mianyang, 621000, China.
Decai WangSchool of Medicine, Mianyang Central Hospital, University of Electronic Science and Technology of China, Mianyang, 621000, China.
Wei WuSouthwest University of Science and Technology, Mianyang, 621010, China.
Mingming TangClinical Medical School, North Sichuan Medical College, Nanchong, 637000, China.
Huayan ZhangSouthwest University of Science and Technology, Mianyang, 621010, China.
Yihan ZhuSchool of Medicine, Mianyang Central Hospital, University of Electronic Science and Technology of China, Mianyang, 621000, China.
Yu ZhangSchool of Medicine, Mianyang Central Hospital, University of Electronic Science and Technology of China, Mianyang, 621000, China.
Yiwei YangInstitute of Applied Electronics, China Academy of Engineering Physics, Mianyang, 621900, China.
Xiaobo DuSchool of Medicine, Mianyang Central Hospital, University of Electronic Science and Technology of China, Mianyang, 621000, China. duxiaobo2005@126.com.

Funding

General Program of the Sichuan Natural Science Foundation 2023NSFSC0710Projects of National Natural Science Foundation of China U2330122
6 · The paper itself

Abstract

purposeUltra-high dose rate (UHDR) radiation retains tumor-killing efficacy while mitigating toxicity to normal tissues, holding a promising transformative radiotherapy paradigm. This study aimed to explore the potential role of mitochondria in intestinal protection conferred by high-energy X-ray FLASH radiotherapy (FLASH-RT) and the associated signaling pathways.

methodHealthy female C57BL/6 mice were subjected to whole-abdominal irradiation using three modalities: ultra-high dose rate radiotherapy (FLASH-RT), conventional dose rate radiotherapy (CONV-RT), and sham irradiation (Control). Mouse survival status and body weight changes were monitored within 15 days post-irradiation. At 72 h post-irradiation, whole blood samples were collected for hematological analysis, and intestinal tissues were harvested for pathological detection, transmission electron microscopy (TEM)-based observation of mitochondrial alterations, and two types of mitochondria-targeted metabolomic assays.

resultsA Compact single High-energy X-ray Source FLASH-RT device (CHEX-FLASH) was used, with a dose rate of 200 Gy/s. At 15 days post-irradiation, the survival rates of the Control group (100%, 10/10) and FLASH-RT group (80%, 8/10) were significantly higher than those of the CONV-RT group (30%, 3/10). Body weight decreased in the early post-irradiation period in all groups; however, the decline was milder in the FLASH-RT group with greater late-stage recovery. Hematological results at 72 h showed that CONV-RT induced similar marrow suppression compared to FLASH-RT. Intestinal histopathological analysis revealed that FLASH-RT alleviated intestinal inflammation and promoted enterocyte proliferation, whereas DNA double-strand breaks and apoptosis levels did not differ significantly between the two irradiated groups. FLASH-RT mitigated mitochondrial damage, reduced reactive oxygen species (ROS) levels and slightly activated mitophagy. Mitochondria-related energy metabolomics detection of intestinal tissues showed that the mitochondrial damage marker malonic acid was significantly lower in FLASH-RT than in CONV-RT, and differentially expressed metabolites were primarily enriched in mitochondrial antioxidant pathways. Additionally, upregulated expression of the antioxidant protein nuclear factor erythroid 2-related factor 2 (NRF2) and decreased total superoxide dismutase (SOD) activity were verified.

conclusionCHEX-FLASH achieves UHDR irradiation and alleviates radiation-induced intestinal injury. The protective effect of FLASH-RT on intestinal tissues may be mediated by mitigating mitochondrial damage and enhancing antioxidant pathways through the improvement of mitochondrial energy metabolism.

Indexed as

IntestinesMitochondriaRadiotherapy, High-EnergyAnimalsFemaleMiceMice, Inbred C57BLRadiation Injuries, ExperimentalX-RaysFLASH effectIntestineMetabolismMitochondriaUltra-high dose rateX-ray

Identifiers

PMID41764525
PMCPMC13059263

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Registered trials

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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.