JOURNAL ARTICLE

Mitochondrial reactive oxygen species-mediated fibroblast activation has a role in tumor microenvironment formation in radiation carcinogenesis.

  • Published In: Radiation Protection Dosimetry, 2024, v. 200, n. 16-18. P. 1590 1 of 3

  • Database: Applied Science & Technology Source Ultimate 2 of 3

  • Authored By: Shimura, Tsutomu; Ushiyama, Akira 3 of 3

Abstract

This article focuses on the role of mitochondria in radiation-induced carcinogenesis, particularly through their involvement in oxidative stress and fibroblast activation within the tumor microenvironment. It highlights that ionizing radiation (IR) causes reactive oxygen species (ROS)-mediated mitochondrial DNA damage, which contributes to both acute tissue injury and long-term cancer risk. The study emphasizes how chronic radiation exposure activates fibroblasts, which can transform into cancer-associated fibroblasts (CAFs) that support tumor growth by interacting with cancer cells. These findings suggest mitochondrial signaling is crucial in radiation carcinogenesis, influencing cell fate and the formation of the tumor microenvironment.

Additional Information

  • Source:Radiation Protection Dosimetry. 2024/11, Vol. 200, Issue 16-18, p1590
  • Document Type:Article
  • Subject Area:History
  • Publication Date:2024
  • ISSN:01448420
  • DOI:10.1093/rpd/ncae027
  • Accession Number:180905344
  • Copyright Statement:Copyright of Radiation Protection Dosimetry is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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