Evidence map›Paper›PMID 33032073›Full record

ArticleRedox biology2020

Involvement of the mitochondrial nuclease EndoG in the regulation of cell proliferation through the control of reactive oxygen species.

Natividad Blasco, Aida Beà, Gisel Barés, Cristina Girón, Raúl Navaridas, Andrea Irazoki, Guillermo López-Lluch, Antonio Zorzano, Xavier Dolcet, Marta Llovera and 1 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  5. Review
  6. Endonuclease G promotes hepatic mitochondrial respiration by selectively increasing mitochondrial tRNAProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Mitochondrial Reactive Oxygen Species (mROS) Generation and Cancer:International journal of nanomedicine · 2025
    Review
  8. Article
  9. Article
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  14. Review
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

11 authors at 3 institutions in 1 country.

Natividad BlascoCell Signaling & Apoptosis Group. Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida-IRBLleida, Lleida, 25198, Spain.
Aida BeàCell Signaling & Apoptosis Group. Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida-IRBLleida, Lleida, 25198, Spain.
Gisel BarésCell Signaling & Apoptosis Group. Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida-IRBLleida, Lleida, 25198, Spain.
Cristina GirónCell Signaling & Apoptosis Group. Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida-IRBLleida, Lleida, 25198, Spain.
Raúl NavaridasOncologic Pathology Group. Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida-IRBLleida, Lleida, 25198, CIBERONC, Spain.
Andrea IrazokiInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST) & CIBERDEM & Departament de Bioquímica I Biomedicina Molecular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain.
Guillermo López-LluchAndalusian Center of Developmental Biology, Pablo de Olavide University, Sevilla, 41013, CIBERER, Spain.
Antonio ZorzanoInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST) & CIBERDEM & Departament de Bioquímica I Biomedicina Molecular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain.
Xavier DolcetOncologic Pathology Group. Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida-IRBLleida, Lleida, 25198, CIBERONC, Spain.
Marta LloveraCell Signaling & Apoptosis Group. Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida-IRBLleida, Lleida, 25198, Spain.
Daniel SanchisCell Signaling & Apoptosis Group. Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida-IRBLleida, Lleida, 25198, Spain. Electronic address: daniel.sanchis@udl.cat.
Universitat de Lleida · ESCentro de Investigación Biomédica en Red · ESUniversidad Pablo de Olavide · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The apoptotic nuclease EndoG is involved in mitochondrial DNA replication. Previous results suggested that, in addition to regulate cardiomyocyte hypertrophy, EndoG could be involved in cell proliferation. Here, by using in vivo and cell culture models, we investigated the role of EndoG in cell proliferation. Genetic deletion of Endog both in vivo and in cultured cells or Endog silencing in vitro induced a defect in rodent and human cell proliferation with a tendency of cells to accumulate in the G

Indexed as

ApoptosisCell ProliferationEndodeoxyribonucleasesMitochondriaReactive Oxygen SpeciesAnimalsCell CycleGlycogen Synthase Kinase 3 betaHEK293 CellsHumansMiceRatsEndodeoxyribonucleasesendonuclease GGlycogen Synthase Kinase 3 betaReactive Oxygen SpeciesCell proliferationCell signalingEndoGHumaninMitochondriaReactive oxygen speciesRomo1

Identifiers

PMID33032073
PMCPMC7552104
OpenAlexW3089265429

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.