Evidence map›Paper›PMID 39425547›Full record

ReviewImmunological reviews2025

A comprehensive review of sensors of radiation-induced damage, radiation-induced proximal events, and cell death.

Saurabh Saini, Prajwal Gurung

Abstract readReview
In one paragraph

Review in Immunological reviews, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Progress in the application ofAnnals of nuclear medicine · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Proton FLASH Exposure Preserves Gut Commensal Microbiomes and Spares Intestinal Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  14. Article
  15. Article
  16. Multifaceted regulation of immune cells in radiation-induced pulmonary fibrosis: from mechanistic insights to targeted therapies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  17. Ferroptosis-induced immune modulation: a new frontier in glioblastoma therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Saurabh SainiInflammation Program, University of Iowa, Iowa City, Iowa, USA.
Prajwal GurungInflammation Program, University of Iowa, Iowa City, Iowa, USA.ORCID 0000-0002-7451-9433

Funding

Implicating a previously unknown Dectin1-RIPK2-CARD9 signaling in providing resistance against Leishmania major infectionR01AI155425 · NIAID · UNIVERSITY OF IOWA · PI GURUNG, PRAJWAL · 2021 to 2025
$2.5M
Elucidating underlying mechanisms in RIPK2-mediated toxicity following exposure to radiationI01BX006091 · VA · IOWA CITY VA MEDICAL CENTER · PI GURUNG, PRAJWAL · 2024 to 2025
–
BLRD VA I01 BX006091NIAID NIH HHS R01 AI155425Prajwal Gurung NIH R01AI155425Prajwal Gurung VA Merit I01BX006091
6 · The paper itself

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.

Indexed as

DNA DamageRadiation InjuriesReceptors, Pattern RecognitionAlarminsAnimalsCell DeathDNA RepairHumansImmunity, InnateRadiation, IonizingReactive Oxygen SpeciesSignal TransductionAlarminsReactive Oxygen SpeciesReceptors, Pattern Recognitioncell deathinnate immunityinnate sensorsradiation

Identifiers

PMID39425547
PMCPMC11742653

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.