Evidence map›Paper›PMID 29099268›Full record

ArticleCell cycle (Georgetown, Tex.)2017

ATM-mediated mitochondrial damage response triggered by nuclear DNA damage in normal human lung fibroblasts.

Tsutomu Shimura, Megumi Sasatani, Hidehiko Kawai, Kenji Kamiya, Junya Kobayashi, Kenshi Komatsu, Naoki Kunugita

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Mitochondrial Signaling Pathways Associated with DNA Damage Responses.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. 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

7 authors at 3 institutions in 1 country.

Tsutomu Shimuraa Department of Environmental Health ; National Institute of Public Health 2-3-6 Minami ; Wako , Saitama , Japan.
Megumi Sasatanib Department of Experimental Oncology ; Research Center for Radiation Genome Medicine ; Research Institute for Radiation Biology and Medicine (RIRBM) ; Hiroshima University , Hiroshima , Japan .
Hidehiko Kawaib Department of Experimental Oncology ; Research Center for Radiation Genome Medicine ; Research Institute for Radiation Biology and Medicine (RIRBM) ; Hiroshima University , Hiroshima , Japan .
Kenji Kamiyab Department of Experimental Oncology ; Research Center for Radiation Genome Medicine ; Research Institute for Radiation Biology and Medicine (RIRBM) ; Hiroshima University , Hiroshima , Japan .
Junya Kobayashic Department of Genome Dynamics , Radiation Biology Center ; Kyoto University ; Kyoto , Japan.
Kenshi Komatsuc Department of Genome Dynamics , Radiation Biology Center ; Kyoto University ; Kyoto , Japan.
Naoki Kunugitaa Department of Environmental Health ; National Institute of Public Health 2-3-6 Minami ; Wako , Saitama , Japan.
Hiroshima University · JPKyoto University · JPNational Institute of Public Health · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ionizing radiation (IR) elevates mitochondrial oxidative phosphorylation (OXPHOS) in response to the energy requirement for DNA damage responses. Reactive oxygen species (ROS) released during mitochondrial OXPHOS may cause oxidative damage to mitochondria in irradiated cells. In this paper, we investigated the association between nuclear DNA damage and mitochondrial damage following IR in normal human lung fibroblasts. In contrast to low-doses of acute single radiation, continuous exposure of chronic radiation or long-term exposure of fractionated radiation (FR) induced persistent Rad51 and γ-H2AX foci at least 24 hours after IR in irradiated cells. Additionally, long-term FR increased mitochondrial ROS accompanied with enhanced mitochondrial membrane potential (ΔΨm) and mitochondrial complex IV (cytochrome c oxidase) activity. Mitochondrial ROS released from the respiratory chain complex I caused oxidative damage to mitochondria. Inhibition of ATM kinase or ATM loss eliminated nuclear DNA damage recognition and mitochondrial radiation responses. Consequently, nuclear DNA damage activates ATM which in turn increases ROS level and subsequently induces mitochondrial damage in irradiated cells. In conclusion, we demonstrated that ATM is essential in the mitochondrial radiation responses in irradiated cells. We further demonstrated that ATM is involved in signal transduction from nucleus to the mitochondria in response to IR.

Indexed as

DNA DamageAdenosine TriphosphateAtaxia Telangiectasia Mutated ProteinsCell LineCell NucleusDNA RepairElectron Transport Complex IFibroblastsHistonesHumansLungMembrane Potential, MitochondrialMitochondriaOxidative PhosphorylationRad51 RecombinaseRadiation, IonizingAdenosine TriphosphateAtaxia Telangiectasia Mutated ProteinsElectron Transport Complex IH2AX protein, humanHistonesRad51 RecombinaseReactive Oxygen SpeciesATMLong-term fractionated radiationmitochondriaparkinROS

Identifiers

PMID29099268
PMCPMC5788412
OpenAlexW2767179221

What OpenQuestion holds

Textmetadata
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.