Evidence map›Paper›PMID 34200499›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Hydroquinone Exposure Worsens Rheumatoid Arthritis through the Activation of the Aryl Hydrocarbon Receptor and Interleukin-17 Pathways.

Cintia Scucuglia Heluany, Paula Barbim Donate, Ayda Henriques Schneider, André Luis Fabris, Renan Augusto Gomes, Isadora Maria Villas-Boas, Denise Vilarinho Tambourgi, Tarcilia Aparecida da Silva, Gustavo Henrique Goulart Trossini, Giovanna Nalesso and 3 more

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 15 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

13 authors at 4 institutions in 2 countries.

Cintia Scucuglia HeluanyDepartment of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.
Paula Barbim DonateDepartment of Pharmacology; Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto 14049-900, Brazil.
Ayda Henriques SchneiderDepartment of Pharmacology; Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto 14049-900, Brazil.
André Luis FabrisDepartment of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.ORCID 0000-0002-1777-2125
Renan Augusto GomesDepartment of Pharmacy, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.
Isadora Maria Villas-BoasImmunochemistry Laboratory, Butantan Institute, São Paulo 05503-900, Brazil.
Denise Vilarinho TambourgiImmunochemistry Laboratory, Butantan Institute, São Paulo 05503-900, Brazil.ORCID 0000-0003-1896-9074
Tarcilia Aparecida da SilvaDepartment of Oral Surgery and Pathology, School of Dentistry, Federal University of Minas Gerais, Belo Horizonte 31.270-901, Brazil.ORCID 0000-0001-9623-7835
Gustavo Henrique Goulart TrossiniDepartment of Pharmacy, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.
Giovanna NalessoDepartment of Pre-Clinical Sciences, School of Veterinary Medicine, University of Surrey, Guildford GU2 7AL, UK.
Eduardo Lani Volpe SilveiraDepartment of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.ORCID 0000-0001-8333-2884
Fernando Queiroz CunhaDepartment of Pharmacology; Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto 14049-900, Brazil.ORCID 0000-0003-4755-1670
Sandra Helena Poliselli FarskyDepartment of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.
Universidade de São Paulo · BRInstituto Butantan · BRUniversidade Federal de Minas Gerais · BRUniversity of Surrey · GB

Funding

Fundação de Amparo à Pesquisa do Estado de São Paulo 2014/07328-4; 2019/19573-7; 2017/26998-9
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) development is strongly associated with cigarette smoke exposure, which activates the aryl hydrocarbon receptor (AhR) as a trigger for Th17 inflammatory pathways. We previously demonstrated that the exposure to hydroquinone (HQ), one of the major compounds of cigarette tar, aggravates the arthritis symptomatology in rats. However, the mechanisms related to the HQ-related RA still remain elusive. Cell viability, cytokine secretion, and gene expression were measured in RA human fibroblast-like synoviocytes (RAHFLS) treated with HQ and stimulated or not with TNF-α. Antigen-induced arthritis (AIA) was also elicited in wild type (WT), AhR

Indexed as

antigen-induced arthritisbenzene metabolitecigarette smokingenvironmental pollutantfibroblast-like synoviocytes

Identifiers

PMID34200499
PMCPMC8229175
OpenAlexW3172656815

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.