Evidence map›Paper›PMID 34681703›Full record

ReviewInternational journal of molecular sciences2021

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

Dietrich Averbeck, Claire Rodriguez-Lafrasse

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed, 1 pooled it
17.8field-weighted citation impact, top 1% of its field
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

121 citing papers in PubMed, 1 synthesis or guideline pooled it, 208 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

61 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Dietrich AverbeckLaboratory of Cellular and Molecular Radiobiology, PRISME, UMR CNRS 5822/IN2P3, IP2I, Lyon-Sud Medical School, University Lyon 1, 69921 Oullins, France.
Claire Rodriguez-LafrasseLaboratory of Cellular and Molecular Radiobiology, PRISME, UMR CNRS 5822/IN2P3, IP2I, Lyon-Sud Medical School, University Lyon 1, 69921 Oullins, France.
Centre National de la Recherche Scientifique · FRHospices Civils de Lyon · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Radiation, IonizingEpigenesis, GeneticEpithelial-Mesenchymal TransitionGenomic InstabilityHumansMitochondriaMitochondrial DynamicsOxidative StressReactive Oxygen SpeciesSignal TransductionReactive Oxygen Speciesadaptive responseapoptosiscancercarbon-ion radiotherapy (CIRT)carbon ionsDNA damage response (DDR)epigeneticsgenomic instabilityhigh LET particle radiationhormesisinnate and adaptive immune responsesionizing radiationmetabolismmitochondrianon-targeted effects (NTEs)radiation qualityradiotherapyROSsignaling

Identifiers

PMID34681703
PMCPMC8541263
OpenAlexW3207922131

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.