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- 1Zunyi Medical University Dental Hospital, Zunyi, China
- 2Zunyi Medical University, Zunyi, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
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
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.