Evidence map›Paper›PMID 25625517›Full record

ReviewInternational journal of molecular sciences2015

Autophagy in DNA damage response.

Piotr Czarny, Elzbieta Pawlowska, Jolanta Bialkowska-Warzecha, Kai Kaarniranta, Janusz Blasiak

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
12.9field-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

93 citing papers in PubMed, 162 citations in OpenAlex.

  1. ADSCs-Exo ameliorates UVB-induced skin DNA damage via p62-RNF168-dependent histone ubiquitination.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026
    Article
  2. Article
  3. A decline in follicle cell function is a major driver ofbioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Autophagy in ocular diseases: from mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
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  15. Article
  16. Deletion ofInternational journal of molecular sciences · 2024
    Article
  17. Review
  18. Review
  19. Article
  20. Article

33 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

5 authors at 3 institutions in 2 countries.

Piotr CzarnyDepartment of Molecular Genetics, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland. pczarny@biol.uni.lodz.pl.
Elzbieta PawlowskaDepartment of Orthodontics, Medical University of Lodz, Pomorska 251, 92-216 Lodz, Poland. elzbieta.pawlowska@umed.lodz.pl.
Jolanta Bialkowska-WarzechaDepartment of Infectious and Liver Diseases, Medical University of Lodz, Kniaziewicza 1/5, 92-347 Lodz, Poland. jbialkowska@pro.onet.pl.
Kai KaarnirantaDepartment of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio FI-70211, Finland. Kai.Kaarniranta@kuh.fi.
Janusz BlasiakDepartment of Molecular Genetics, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland. jblasiak@biol.uni.lodz.pl.
Medical University of Lodz · PLUniversity of Łódź · PLKuopio University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage response (DDR) involves DNA repair, cell cycle regulation and apoptosis, but autophagy is also suggested to play a role in DDR. Autophagy can be activated in response to DNA-damaging agents, but the exact mechanism underlying this activation is not fully understood, although it is suggested that it involves the inhibition of mammalian target of rapamycin complex 1 (mTORC1). mTORC1 represses autophagy via phosphorylation of the ULK1/2-Atg13-FIP200 complex thus preventing maturation of pre-autophagosomal structures. When DNA damage occurs, it is recognized by some proteins or their complexes, such as poly(ADP)ribose polymerase 1 (PARP-1), Mre11-Rad50-Nbs1 (MRN) complex or FOXO3, which activate repressors of mTORC1. SQSTM1/p62 is one of the proteins whose levels are regulated via autophagic degradation. Inhibition of autophagy by knockout of FIP200 results in upregulation of SQSTM1/p62, enhanced DNA damage and less efficient damage repair. Mitophagy, one form of autophagy involved in the selective degradation of mitochondria, may also play role in DDR. It degrades abnormal mitochondria and can either repress or activate apoptosis, but the exact mechanism remains unknown. There is a need to clarify the role of autophagy in DDR, as this process may possess several important biomedical applications, involving also cancer therapy.

Indexed as

AutophagyDNA RepairAdaptor Proteins, Signal TransducingAntineoplastic AgentsDNA DamageForkhead Transcription FactorsHumansMitochondriaNeoplasmsRadiation, IonizingSequestosome-1 ProteinTOR Serine-Threonine KinasesTumor Suppressor Protein p53Adaptor Proteins, Signal TransducingAntineoplastic AgentsForkhead Transcription FactorsSequestosome-1 ProteinSQSTM1 protein, humanTOR Serine-Threonine KinasesTumor Suppressor Protein p53

Identifiers

PMID25625517
PMCPMC4346856
OpenAlexW2107078346

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.