Evidence map›Paper›PMID 36552527›Full record

ReviewAntioxidants (Basel, Switzerland)2022

Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review.

Marina M Tavleeva, Elena S Belykh, Anna V Rybak, Elena E Rasova, Aleksey A Chernykh, Zaur B Ismailov, Ilya O Velegzhaninov

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  3. Mechanistic signatures of comorbid PTSD with cognitive impairment implicate cortisol-induced neural toxicity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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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

7 authors at 2 institutions in 1 country.

Marina M TavleevaInstitute of Biology of Komi Scientific Centre, Ural Branch of Russian Academy of Sciences, 28b Kommunisticheskaya St., Syktyvkar 167982, Russia.
Elena S BelykhInstitute of Biology of Komi Scientific Centre, Ural Branch of Russian Academy of Sciences, 28b Kommunisticheskaya St., Syktyvkar 167982, Russia.
Anna V RybakInstitute of Biology of Komi Scientific Centre, Ural Branch of Russian Academy of Sciences, 28b Kommunisticheskaya St., Syktyvkar 167982, Russia.
Elena E RasovaInstitute of Biology of Komi Scientific Centre, Ural Branch of Russian Academy of Sciences, 28b Kommunisticheskaya St., Syktyvkar 167982, Russia.
Aleksey A ChernykhInstitute of Physiology of Komi Scientific Centre, Ural Branch of Russian Academy of Sciences, 50 Pervomaiskaya St., Syktyvkar 167982, Russia.
Zaur B IsmailovInstitute of Biology of Komi Scientific Centre, Ural Branch of Russian Academy of Sciences, 28b Kommunisticheskaya St., Syktyvkar 167982, Russia.ORCID 0000-0002-2686-3424
Ilya O VelegzhaninovInstitute of Biology of Komi Scientific Centre, Ural Branch of Russian Academy of Sciences, 28b Kommunisticheskaya St., Syktyvkar 167982, Russia.ORCID 0000-0002-4715-4053
Institute of Biology of Komi Scientific Centre · RURussian Academy of Sciences · RU

Funding

Russian Science Foundation 22-24-01042
6 · The paper itself

Abstract

Reactive oxygen species (ROS) are normal products of a number of biochemical reactions and are important signaling molecules. However, at the same time, they are toxic to cells and have to be strictly regulated by their antioxidant systems. The etiology and pathogenesis of many diseases are associated with increased ROS levels, and many external stress factors directly or indirectly cause oxidative stress in cells. Within this context, the overexpression of genes encoding the proteins in antioxidant systems seems to have become a viable approach to decrease the oxidative stress caused by pathological conditions and to increase cellular stress resistance. However, such manipulations unavoidably lead to side effects, the most dangerous of which is an increased probability of healthy tissue malignization or increased tumor aggression. The aims of the present review were to collect and systematize the results of studies devoted to the effects resulting from the overexpression of antioxidant system genes on stress resistance and carcinogenesis in vitro and in vivo. In most cases, the overexpression of these genes was shown to increase cell and organism resistances to factors that induce oxidative and genotoxic stress but to also have different effects on cancer initiation and promotion. The last fact greatly limits perspectives of such manipulations in practice. The overexpression of

Indexed as

antioxidant genescarcinogenesisgene therapyoncosuppressionoverexpressionstress resistance

Identifiers

PMID36552527
PMCPMC9774954
OpenAlexW4309848148

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.