Evidence map›Paper›PMID 29112132›Full record

ReviewInternational journal of molecular sciences2017

Autophagy Roles in the Modulation of DNA Repair Pathways.

Luciana R Gomes, Carlos F M Menck, Giovana S Leandro

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 134 citations in OpenAlex.

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  5. A decline in follicle cell function is a major driver ofbioRxiv : the preprint server for biology · 2026
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8 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

3 authors at 1 institution in 1 country.

Luciana R GomesDepartment of Microbiology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo 05508-900, SP, Brazil. luciana.gomes@usp.br.
Carlos F M MenckDepartment of Microbiology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo 05508-900, SP, Brazil. cfmmenck@usp.br.
Giovana S LeandroDepartment of Microbiology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo 05508-900, SP, Brazil. giovanasl@usp.br.
Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy and DNA repair are biological processes vital for cellular homeostasis maintenance and when dysfunctional, they lead to several human disorders including premature aging, neurodegenerative diseases, and cancer. The interchange between these pathways is complex and it may occur in both directions. Autophagy is activated in response to several DNA lesions types and it can regulate different mechanisms and molecules involved in DNA damage response (DDR), such as cell cycle checkpoints, cell death, and DNA repair. Thus, autophagy may modulate DNA repair pathways, the main focus of this review. In addition to the already well-documented autophagy positive effects on homologous recombination (HR), autophagy has also been implicated with other DNA repair mechanisms, such as base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR). Given the relevance of these cellular processes, the clinical applications of drugs targeting this autophagy-DNA repair interface emerge as potential therapeutic strategies for many diseases, especially cancer.

Indexed as

AnimalsAutophagyDNA End-Joining RepairDNA RepairHomologous RecombinationHumansautophagybase excision repair (BER)DNA repairhomologous recombination (HR)non-homologous end joining (NHEJ)nucleotide excision repair (NER)

Identifiers

PMID29112132
PMCPMC5713320
OpenAlexW2767499464

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.