Evidence map›Paper›PMID 29181628›Full record

ReviewCurrent genetics2018

The major contribution of the DNA damage-triggered reactive oxygen species production to cell death: implications for antimicrobial and cancer therapy.

Ivan Matic

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
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  4. A splice site mutation in theHorticulture research · 2023
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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

1 author at 1 institution in 2 countries.

Ivan MaticFaculté de Médecine Paris Descartes, INSERM U1001, Université Paris Descartes, Sorbonne Paris Cité, 24 rue du Faubourg Saint-Jacques, Paris, 75014, France. ivan.matic@inserm.fr.ORCID http://orcid.org/0000-0003-0393-1241
Délégation Paris 5 · FR

Funding

Agence Nationale de la Recherche Idex ANR-11-IDEX-0005-01 / ANR-11-LABX-0071Fondation pour la Recherche Médicale DBF20160635736
6 · The paper itself

Abstract

Genotoxic agents damage DNA, block DNA replication and provoke cell death. However, there is growing evidence that an important part of their cytotoxicity results from metabolic disturbances induced by treatment. This review article describes how increased production of the reactive oxygen species (ROS) induced by different genotoxic agents contribute to death of prokaryotic and eukaryotic cells. ROS are byproducts of normal cellular functioning. Because ROS are damaging cellular macromolecules, they are constantly eliminated by protective antioxidant mechanisms. However, even a small increase in ROS production may have deleterious consequences because cells possess just enough defensive mechanisms to protect themselves against endogenously produced ROS. Therefore, it may be possible to enhance cytotoxic potential of antimicrobial and anticancer drugs by increasing ROS production or by inhibiting cellular antioxidant systems.

Indexed as

Cell DeathDNA DamageAnti-Bacterial AgentsAntineoplastic AgentsAntioxidantsBacterial InfectionsHumansNeoplasmsReactive Oxygen SpeciesAnti-Bacterial AgentsAntineoplastic AgentsAntioxidantsReactive Oxygen SpeciesCytotoxicityDNA damageDNA replication blockageGenotoxic agentsReactive oxygen species

Identifiers

PMID29181628
OpenAlexW2769662556

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.