Evidence map›Paper›PMID 35659346›Full record

ArticleArthritis research & therapy2022

Semaphorin 3G exacerbates joint inflammation through the accumulation and proliferation of macrophages in the synovium.

Jumpei Shoda, Shigeru Tanaka, Keishi Etori, Koto Hattori, Tadamichi Kasuya, Kei Ikeda, Yuko Maezawa, Akira Suto, Kotaro Suzuki, Junichi Nakamura and 6 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

10 citing papers in PubMed, 23 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

16 authors at 3 institutions in 2 countries.

Jumpei Shoda *Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Shigeru Tanaka *Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Keishi EtoriDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Koto HattoriDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Tadamichi KasuyaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Kei IkedaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Yuko MaezawaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Akira SutoDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Kotaro SuzukiDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Junichi NakamuraDepartment of Orthopedic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Yoshiro MaezawaDepartment of Endocrinology, Hematology, and Gerontology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Minoru TakemotoDepartment of Endocrinology, Hematology, and Gerontology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Christer BetsholtzDepartment of Immunology, Genetics and Pathology (IGP), Uppsala University, Uppsala, Sweden.
Koutaro YokoteDepartment of Endocrinology, Hematology, and Gerontology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Seiji OhtoriDepartment of Orthopedic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Hiroshi NakajimaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan. nakajimh@faculty.chiba-u.jp.
Chiba University · JPInternational University of Health and Welfare · JPUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesMethotrexate (MTX) is an anchor drug for the treatment of rheumatoid arthritis (RA). However, the precise mechanisms by which MTX stalls RA progression and alleviates the ensuing disease effects remain unknown. The aim of the present study was to identify novel therapeutic target molecules, the expression patterns of which are affected by MTX in patients with RA.

methodsCD4

resultsSemaphorin 3G expression in CD4

conclusionsUpregulation of semaphorin 3G in the RA synovium is a novel mechanism that exacerbates joint inflammation, leading to further deterioration, through macrophage accumulation.

Indexed as

Arthritis, ExperimentalArthritis, RheumatoidSemaphorinsAnimalsCell ProliferationCollagenHumansInflammationMacrophagesMethotrexateMiceNeuropilin-2Synovial MembraneCollagenMethotrexateNeuropilin-2SemaphorinsMacrophageMethotrexateNeuropilin-2Rheumatoid arthritisSemaphorin

Identifiers

PMID35659346
PMCPMC9166515
OpenAlexW4281606626

What Socratic 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 Socratic graph.