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Updated: Feb 26, 2026

Intestinal Epithelial Regeneration in Response to Ionizing Irradiation
Published on: July 27, 2022
Mitochondrial function-related genes and ionizing radiation-induced intestinal injury: mechanisms and research
Zhongwei Zhang1, Jun Liu1, Qing-Jie Liu1
1China CDC Key Laboratory of Radiological Protection and Nuclear Emergency, National Institute for Radiological Protection, Chinese Center for Disease Control and Prevention, Beijing, China.
Purpose:
Ionizing radiation-induced intestinal injury (RIII) is a significant complication of radiotherapy and nuclear radiation incidents. Mitochondria, the centers of energy metabolism and apoptosis, are pivotal in the pathogenesis of RIII. Under irradiation conditions, multiple mitochondrial function-related genes modulate the production of reactive oxygen species and ATP, maintain mitochondrial DNA, induce mitophagy, and activate the apoptotic pathway associated with mitochondrial dysfunction, leading to intestinal tissue injury. Mitochondrial function-related genes are pivotal in maintaining the normal function of mitochondria and moderate RIII. This review summarizes the mechanisms of mitochondrial function-related genes in RIII and potential therapeutic strategies, aiming to provide references for further research on RIII and clinical prevention and treatment.
Conclusion:
Mitochondrial dysfunction driven by the dysregulation of genes related to mitochondrial function (nuclear genes and mitochondrial genome) is a key mechanism of RIII pathogenesis. At present, research on pivotal regulators remains limited, necessitating deeper investigation with multi-omics approaches. Precisely targeting these mitochondrial function-related genes offers a promising therapeutic strategy for reducing mitochondrial damage and treating RIII.
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