Journal article
A comprehensive review of sensors of radiation-induced damage, radiation-induced proximal events, and cell death
Immunological reviews, Vol.329(1), e13409
01/18/2025
DOI: 10.1111/imr.13409
PMCID: PMC11742653
PMID: 39425547
Appears in UI Libraries Support Open Access
Abstract
Radiation, a universal component of Earth's environment, is categorized into non-ionizing and ionizing forms. While non-ionizing radiation is relatively harmless, ionizing radiation possesses sufficient energy to ionize atoms and disrupt DNA, leading to cell damage, mutation, cancer, and cell death. The extensive use of radionuclides and ionizing radiation in nuclear technology and medical applications has sparked global concern for their capacity to cause acute and chronic illnesses. Ionizing radiation induces DNA damage either directly through strand breaks and base change or indirectly by generating reactive oxygen species (ROS) and reactive nitrogen species (RNS) via radiolysis of water. This damage triggers a complex cellular response involving recognition of DNA damage, cell cycle arrest, DNA repair mechanisms, release of pro-inflammatory cytokines, and cell death. This review focuses on the mechanisms of radiation-induced cellular damage, recognition of DNA damage and subsequent activation of repair processes, and the critical role of the innate immune response in resolution of the injury. Emphasis is placed on pattern recognition receptors (PRRs) and related receptors that detect damage-associated molecular patterns (DAMPs) and initiate downstream signaling pathways. Radiation-induced cell death pathways are discussed in detail. Understanding these processes is crucial for developing strategies to mitigate the harmful effects of radiation and improve therapeutic outcomes.Radiation, a universal component of Earth's environment, is categorized into non-ionizing and ionizing forms. While non-ionizing radiation is relatively harmless, ionizing radiation possesses sufficient energy to ionize atoms and disrupt DNA, leading to cell damage, mutation, cancer, and cell death. The extensive use of radionuclides and ionizing radiation in nuclear technology and medical applications has sparked global concern for their capacity to cause acute and chronic illnesses. Ionizing radiation induces DNA damage either directly through strand breaks and base change or indirectly by generating reactive oxygen species (ROS) and reactive nitrogen species (RNS) via radiolysis of water. This damage triggers a complex cellular response involving recognition of DNA damage, cell cycle arrest, DNA repair mechanisms, release of pro-inflammatory cytokines, and cell death. This review focuses on the mechanisms of radiation-induced cellular damage, recognition of DNA damage and subsequent activation of repair processes, and the critical role of the innate immune response in resolution of the injury. Emphasis is placed on pattern recognition receptors (PRRs) and related receptors that detect damage-associated molecular patterns (DAMPs) and initiate downstream signaling pathways. Radiation-induced cell death pathways are discussed in detail. Understanding these processes is crucial for developing strategies to mitigate the harmful effects of radiation and improve therapeutic outcomes.
Details
- Title: Subtitle
- A comprehensive review of sensors of radiation-induced damage, radiation-induced proximal events, and cell death
- Creators
- Saurabh Saini - University of Iowa, Internal MedicinePrajwal Gurung - University of Iowa
- Resource Type
- Journal article
- Publication Details
- Immunological reviews, Vol.329(1), e13409
- DOI
- 10.1111/imr.13409
- PMID
- 39425547
- PMCID
- PMC11742653
- NLM abbreviation
- Immunol Rev
- ISSN
- 1600-065X
- eISSN
- 1600-065X
- Publisher
- Wiley
- Grant note
- Prajwal Gurung: I01BX006091, R01AI155425
We thank Ms. Kristina Greiner for her editing assistance in preparing our manuscript. We have tried our best to cite all relevant studies, but sincerely apologize to those whose literature we may have missed. This work was supported by VA Merit I01BX006091, NIH R01AI155425, University of Iowa Startup Funds, and University of Iowa ISP Award to PG.
- Language
- English
- Electronic publication date
- 10/19/2024
- Date published
- 01/18/2025
- Academic Unit
- Infectious Diseases; Internal Medicine
- Record Identifier
- 9984736747302771
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