文献类型：期刊文献

英文题名：Unraveling Radiation Enteritis: Oxidative Stress as a Central Driver and Therapeutic Target

作者：Zhong, Pengfei[1];Li, Zhiyuan[1];Pu, Zhenjun[1];Nian, Hongyu[1];Li, Junliang[1,2,3]

第一作者：Zhong, Pengfei

通信作者：Li, JL[1]

机构：[1]Gansu Univ Chinese Med, Sch Clin Med 1, Gansu Prov Hosp, Lanzhou, Peoples R China;[2]Gansu Prov Hosp, Dept Gen Surg, 204 Donggang West Rd, Lanzhou 730000, Gansu, Peoples R China;[3]Chinese Acad Sci, Inst Modern Phys, Lanzhou, Peoples R China

第一机构：甘肃中医药大学

通信机构：[1]corresponding author), Gansu Prov Hosp, Dept Gen Surg, 204 Donggang West Rd, Lanzhou 730000, Gansu, Peoples R China.

年份：2026

外文期刊名：ANTIOXIDANTS & REDOX SIGNALING

收录：;Scopus(收录号：2-s2.0-105048040557);WOS:【SCI-EXPANDED(收录号:WOS:001853980400001)】；

基金：This work was supported by the National Natural Science Foundation of China(82560595), Gansu Provincial Joint Research Fund (25JRRA1200), Health Industry Research Project of Gansu Province (GSWSQNYPY2024-01), Chengguan District Lanzhou Science and Technology Program (2024RCCX0009), Lanzhou Science and Technology Program Project (2024-9-4), Postgraduate Innovation and Entrepreneurship Fund of Gansu University of Chinese Medicine (2025CXCY-079, 2025CXCY-084, 2026CXCY-051, 2026CXCY-053, 2026CXCY-071), and Hospital Research Fund Project of Gansu Provincial Hospital(24GSSYH-3, 25GSSYK-1).

语种：英文

外文关键词：radiation enteritis; oxidative stress; reactive oxygen species; intestinal microenvironment; radiotherapy; antioxidant therapy

摘要：Significance: Radiation enteritis (RE) is a prevalent complication following abdominopelvic radiotherapy (RT), significantly compromising patients' quality of life. Oxidative stress extends beyond merely mediating early tissue injury; it acts as the central regulatory axis orchestrating sequential pathological transitions, encompassing epithelial damage, immune activation, chronic ischemia, and fibrotic remodeling.Recent Advances: RT-induced reactive oxygen species (ROS) burst provokes lipid peroxidation, mitochondrial dysfunction, programmed cell death, and epithelial barrier disruption. Subsequently, damage-associated molecular pattern release and microbial translocation propel immune-inflammatory amplification. Sustained ROS generation and ensuing inflammation further compromise the vascular endothelium, precipitating microcirculatory dysfunction and chronic hypoxia. Concurrently, barrier disruption and microbial dysbiosis form a feedback loop shifting sustained regenerative responses toward maladaptive repair, ultimately culminating in irreversible tissue remodeling.Critical Issues: Pathogenically, RE is not simply a consequence of ROS overload, but an ROS-driven continuum of tissue state transitions resulting in regenerative failure. Furthermore, a "redox paradox" emerges wherein ROS concurrently drive normal intestinal injury and mediate RT's tumoricidal efficacy. Currently, regenerative failure and this redox paradox remain inadequately integrated into clinical paradigms for patient stratification, interventional timing, and efficacy evaluation.Future Directions: Future endeavors must prioritize precision redox therapeutics characterized by tissue specificity, temporal regulation, and dose-dependent modulation. Leveraging targeted delivery, phased interventions, and biomarkers will reconcile the conflicting demands of normal tissue radioprotection and tumor control, propelling the paradigm shift from broad-spectrum antioxidants toward precision redox medicine. Antioxid. Redox Signal. 00, 000-000.