Evidence map›Paper›PMID 33641680›Full record

ReviewInflammation and regeneration2021

Multiomics landscape of synovial fibroblasts in rheumatoid arthritis.

Haruka Tsuchiya, Mineto Ota, Keishi Fujio

Open access · goldAbstract readReview
In one paragraph

Review in Inflammation and regeneration, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.6field-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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 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

3 authors at 2 institutions in 1 country.

Haruka TsuchiyaDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Mineto OtaDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan.
Keishi FujioDepartment of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan. fujiok-int@h.u-tokyo.ac.jp.ORCID http://orcid.org/0000-0001-7276-5254
The University of Tokyo · JPTokyo Fuji University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is an autoimmune disease characterized by tumor-like hyperplasia and inflammation of the synovium, which causes synovial cell invasion into the bone and cartilage. In RA pathogenesis, various molecules in effector cells (i.e., immune cells and mesenchymal cells) are dysregulated by genetic and environmental factors. Synovial fibroblasts (SFs), the most abundant resident mesenchymal cells in the synovium, are the major local effectors of the destructive joint inflammation and exert their effects through the pathogenic production of molecules such as interleukin-6. MAIN BODY: To date, more than 100 RA susceptibility loci have been identified in genome-wide association studies (GWASs), and finding novel therapeutic targets utilizing genome analysis is considered a promising approach because some candidate causal genes identified by GWASs have previously been established as therapeutic targets. For further exploration of RA-responsible cells and cell type-specific therapeutic targets, integrated analysis (or functional genome analysis) of the genome and intermediate traits (e.g., transcriptome and epigenome) is crucial.

conclusionThis review builds on the existing knowledge regarding the epigenomic abnormalities in RASFs and discusses the recent advances in single-cell analysis, highlighting the prospects of SFs as targets for safer and more effective therapies against RA.

Indexed as

DNA methylationEpigenomeGenomeGenome analysisHistone acetylationIntegrated analysisRheumatoid arthritisSingle-cell analysisSynovial fibroblastsTranscriptome

Identifiers

PMID33641680
PMCPMC7919303
OpenAlexW3133983361

What OpenQuestion holds

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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.