Evidence map›Paper›PMID 23764844›Full record

ArticleCell death & disease2013

Gamma rays induce a p53-independent mitochondrial biogenesis that is counter-regulated by HIF1α.

A Bartoletti-Stella, E Mariani, I Kurelac, A Maresca, M F Caratozzolo, L Iommarini, V Carelli, L H Eusebi, A Guido, G Cenacchi and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Role of p53 in Regulating Radiation Responses.Life (Basel, Switzerland) · 2022
    Review
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  7. Review
  8. Article
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  10. Article
  11. Article
  12. Review
  13. Profiles of Radioresistance Mechanisms in Prostate Cancer.Critical reviews in oncogenesis · 2018
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
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  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

15 authors at 4 institutions in 1 country.

A Bartoletti-StellaMedical Genetics Unit, Department of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy.
E Mariani
I Kurelac
A Maresca
M F Caratozzolo
L Iommarini
V Carelli
L H Eusebi
A Guido
G Cenacchi
L Fuccio
M Rugolo
A Tullo
A M Porcelli
G Gasparre
University of Bologna · ITInstitute of Biomedical Technologies · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITIstituto delle Scienze Neurologiche di Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial biogenesis is an orchestrated process that presides to the regulation of the organelles homeostasis within a cell. We show that γ-rays, at doses commonly used in the radiation therapy for cancer treatment, induce an increase in mitochondrial mass and function, in response to a genotoxic stress that pushes cells into senescence, in the presence of a functional p53. Although the main effector of the response to γ-rays is the p53-p21 axis, we demonstrated that mitochondrial biogenesis is only indirectly regulated by p53, whose activation triggers a murine double minute 2 (MDM2)-mediated hypoxia-inducible factor 1α (HIF1α) degradation, leading to the release of peroxisome-proliferator activated receptor gamma co-activator 1β inhibition by HIF1α, thus promoting mitochondrial biogenesis. Mimicking hypoxia by HIF1α stabilization, in fact, blunts the mitochondrial response to γ-rays as well as the induction of p21-mediated cell senescence, indicating prevalence of the hypoxic over the genotoxic response. Finally, we also show in vivo that post-radiotherapy mitochondrial DNA copy number increase well correlates with lack of HIF1α increase in the tissue, concluding this may be a useful molecular tool to infer the trigger of a hypoxic response during radiotherapy, which may lead to failure of activation of cell senescence.

Indexed as

Mitochondrial TurnoverBase SequenceBinding SitesCarrier ProteinsCell ShapeCellular SenescenceDNA Copy Number VariationsDNA, MitochondrialGene Expression RegulationGenome, MitochondrialHCT116 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitMitochondriaMolecular Sequence DataMutation, MissenseCarrier ProteinsDNA, MitochondrialHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMDM2 protein, humanPPARGC1B protein, humanProto-Oncogene Proteins c-mdm2RNA-Binding ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID23764844
PMCPMC3702280
OpenAlexW2022657565

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.