Evidence map›Paper›PMID 37904059›Full record

ReviewCellular and molecular life sciences : CMLS2023

Mechanisms of genotoxicity and proteotoxicity induced by the metalloids arsenic and antimony.

Robert Wysocki, Joana I Rodrigues, Ireneusz Litwin, Markus J Tamás

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

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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

4 authors at 2 institutions in 2 countries.

Robert WysockiDepartment of Genetics and Cell Physiology, Faculty of Biological Sciences, University of Wroclaw, 50-328, Wroclaw, Poland. robert.wysocki@uwr.edu.pl.ORCID http://orcid.org/0000-0002-3274-2629
Joana I RodriguesDepartment of Chemistry and Molecular Biology, University of Gothenburg, Box 462, 405 30, Göteborg, Sweden.ORCID http://orcid.org/0000-0002-0503-1303
Ireneusz LitwinAcademic Excellence Hub - Research Centre for DNA Repair and Replication, Faculty of Biological Sciences, University of Wroclaw, 50-328, Wroclaw, Poland.ORCID http://orcid.org/0000-0002-2764-0708
Markus J TamásDepartment of Chemistry and Molecular Biology, University of Gothenburg, Box 462, 405 30, Göteborg, Sweden. markus.tamas@cmb.gu.se.ORCID http://orcid.org/0000-0002-0762-7848
University of Gothenburg · SEUniversity of Wrocław · PL

Funding

Narodowe Centrum Nauki 2016/21/B/NZ2/01751Vetenskapsrådet 2018-03577
6 · The paper itself

Abstract

Arsenic and antimony are metalloids with profound effects on biological systems and human health. Both elements are toxic to cells and organisms, and exposure is associated with several pathological conditions including cancer and neurodegenerative disorders. At the same time, arsenic- and antimony-containing compounds are used in the treatment of multiple diseases. Although these metalloids can both cause and cure disease, their modes of molecular action are incompletely understood. The past decades have seen major advances in our understanding of arsenic and antimony toxicity, emphasizing genotoxicity and proteotoxicity as key contributors to pathogenesis. In this review, we highlight mechanisms by which arsenic and antimony cause toxicity, focusing on their genotoxic and proteotoxic effects. The mechanisms used by cells to maintain proteostasis during metalloid exposure are also described. Furthermore, we address how metalloid-induced proteotoxicity may promote neurodegenerative disease and how genotoxicity and proteotoxicity may be interrelated and together contribute to proteinopathies. A deeper understanding of cellular toxicity and response mechanisms and their links to pathogenesis may promote the development of strategies for both disease prevention and treatment.

Indexed as

ArsenicMetalloidsNeurodegenerative DiseasesAntimonyDNA DamageHumansAntimonyArsenicMetalloidsAntimony toxicityArsenic toxicityGenotoxicityMetalloidProtein aggregationProtein foldingProteostasisProteotoxicity

Identifiers

PMID37904059
PMCPMC10616229
OpenAlexW4388018115

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.