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REVIEW article

Front. Physiol.

Sec. Mitochondrial Research

Volume 16 - 2025 | doi: 10.3389/fphys.2025.1660330

This article is part of the Research TopicMitochondria as Integrative Signaling Hubs in Cellular Stress ResponsesView all articles

Advances in mitochondrial dysfunction in radiation tissue injury

Provisionally accepted
Jianhuang  RongJianhuang Rong1Nini  ZhangNini Zhang1*Qiujie  YuQiujie Yu2Guilin  HuangGuilin Huang1
  • 1Zunyi Medical University Dental Hospital, Zunyi, China
  • 2Zunyi Medical University, Zunyi, China

The final, formatted version of the article will be published soon.

Radiation-induced tissue injury is a major limitation in cancer radiotherapy, often leading to collateral damage in healthy tissues. While the nucleus has long been considered the principal target of ionizing radiation, emerging evidence underscores the pivotal role of mitochondria in mediating radiation-induced damage. This review provides a comprehensive overview of mitochondrial dysfunction in various irradiated tissues, including the intestine, hematopoietic system, heart, lung, brain, and skin. Key mitochondrial alterationssuch as disrupted dynamics, impaired energy metabolism, excessive reactive oxygen species (ROS) production, and activation of apoptotic and senescence pathwaysare highlighted as central mechanisms underlying radiation pathology.Additionally, we summarize the involvement of crucial signaling pathways such as AMP-activated protein kinase/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (AMPK/PGC-1 α ),nuclear factor erythroid 2related factor 2/antioxidant response element/mitochondrial transcription factor A (Nrf2/ARE/TFAM), and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in regulating mitochondrial responses to radiation stress. A deeper understanding of mitochondrial involvement provides novel avenues for radioprotection and therapeutic interventions in oncology.

Keywords: Mitochondrial dysfunction, radiation injury, Oxidative Stress, mitophagy, Apoptosis, Energy Metabolism

Received: 05 Jul 2025; Accepted: 06 Aug 2025.

Copyright: © 2025 Rong, Zhang, Yu and Huang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Nini Zhang, Zunyi Medical University Dental Hospital, Zunyi, China

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