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Review

Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts

1
Laboratory of Cellular and Molecular Radiobiology, PRISME, UMR CNRS 5822/IN2P3, IP2I, Lyon-Sud Medical School, University Lyon 1, 69921 Oullins, France
2
Department of Biochemistry and Molecular Biology, Lyon-Sud Hospital, Hospices Civils de Lyon, 69310 Pierre-Bénite, France
*
Author to whom correspondence should be addressed.
Academic Editors: Mauro Belli and Antonella Sgura
Int. J. Mol. Sci. 2021, 22(20), 11047; https://doi.org/10.3390/ijms222011047
Received: 12 August 2021 / Revised: 24 September 2021 / Accepted: 8 October 2021 / Published: 13 October 2021
(This article belongs to the Special Issue Epigenetic Effects and Non-DNA Targets of Ionizing Radiation)
Until recently, radiation effects have been considered to be mainly due to nuclear DNA damage and their management by repair mechanisms. However, molecular biology studies reveal that the outcomes of exposures to ionizing radiation (IR) highly depend on activation and regulation through other molecular components of organelles that determine cell survival and proliferation capacities. As typical epigenetic-regulated organelles and central power stations of cells, mitochondria play an important pivotal role in those responses. They direct cellular metabolism, energy supply and homeostasis as well as radiation-induced signaling, cell death, and immunological responses. This review is focused on how energy, dose and quality of IR affect mitochondria-dependent epigenetic and functional control at the cellular and tissue level. Low-dose radiation effects on mitochondria appear to be associated with epigenetic and non-targeted effects involved in genomic instability and adaptive responses, whereas high-dose radiation effects (>1 Gy) concern therapeutic effects of radiation and long-term outcomes involving mitochondria-mediated innate and adaptive immune responses. Both effects depend on radiation quality. For example, the increased efficacy of high linear energy transfer particle radiotherapy, e.g., C-ion radiotherapy, relies on the reduction of anastasis, enhanced mitochondria-mediated apoptosis and immunogenic (antitumor) responses. View Full-Text
Keywords: ionizing radiation; high LET particle radiation; carbon ions; radiation quality; ROS; mitochondria; epigenetics; metabolism; signaling; DNA damage response (DDR); hormesis; adaptive response; apoptosis; non-targeted effects (NTEs); genomic instability; cancer; innate and adaptive immune responses; radiotherapy; carbon-ion radiotherapy (CIRT) ionizing radiation; high LET particle radiation; carbon ions; radiation quality; ROS; mitochondria; epigenetics; metabolism; signaling; DNA damage response (DDR); hormesis; adaptive response; apoptosis; non-targeted effects (NTEs); genomic instability; cancer; innate and adaptive immune responses; radiotherapy; carbon-ion radiotherapy (CIRT)
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MDPI and ACS Style

Averbeck, D.; Rodriguez-Lafrasse, C. Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts. Int. J. Mol. Sci. 2021, 22, 11047. https://doi.org/10.3390/ijms222011047

AMA Style

Averbeck D, Rodriguez-Lafrasse C. Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts. International Journal of Molecular Sciences. 2021; 22(20):11047. https://doi.org/10.3390/ijms222011047

Chicago/Turabian Style

Averbeck, Dietrich, and Claire Rodriguez-Lafrasse. 2021. "Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts" International Journal of Molecular Sciences 22, no. 20: 11047. https://doi.org/10.3390/ijms222011047

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