Evidence map›Paper›PMID 29784872›Full record

ArticleBioscience reports2018

SIRT1 inhibits rheumatoid arthritis fibroblast-like synoviocyte aggressiveness and inflammatory response via suppressing NF-κB pathway.

Guoqing Li, Zhongbing Xia, Ying Liu, Fanru Meng, Xia Wu, Yuxuan Fang, Chunwang Zhang, Dan Liu

Expression of concernOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bioscience reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
4.2field-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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

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  18. Role of Sirtuins in the Pathogenesis of Rheumatoid Arthritis.International journal of molecular sciences · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Guoqing LiDepartment of Rheumatology, Northern Jiangsu People's Hospital affiliated to Yangzhou University, Yangzhou City, Jiangsu Province 225000, P.R. China.
Zhongbing XiaDepartment of Rheumatology, Northern Jiangsu People's Hospital affiliated to Yangzhou University, Yangzhou City, Jiangsu Province 225000, P.R. China.
Ying LiuDepartment of Rheumatology, Northern Jiangsu People's Hospital affiliated to Yangzhou University, Yangzhou City, Jiangsu Province 225000, P.R. China.
Fanru MengDepartment of Rheumatology, Northern Jiangsu People's Hospital affiliated to Yangzhou University, Yangzhou City, Jiangsu Province 225000, P.R. China.
Xia WuDepartment of Rheumatology, Northern Jiangsu People's Hospital affiliated to Yangzhou University, Yangzhou City, Jiangsu Province 225000, P.R. China.
Yuxuan FangDepartment of Rheumatology, Northern Jiangsu People's Hospital affiliated to Yangzhou University, Yangzhou City, Jiangsu Province 225000, P.R. China.
Chunwang ZhangDepartment of Rheumatology, Northern Jiangsu People's Hospital affiliated to Yangzhou University, Yangzhou City, Jiangsu Province 225000, P.R. China.
Dan LiuDepartment of Pathology, Northern Jiangsu People's Hospital affiliated to Yangzhou University, Yangzhou City, Jiangsu Province 225000, P.R. China g53a8x4nq0h52@163.com.
Northern Jiangsu People's Hospital · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune disease of the joints characterized by synovial hyperplasia and chronic inflammation. Fibroblast-like synoviocytes (FLS) play a central role in RA initiation, progression, and perpetuation. Prior studies showed that sirtuin 1 (SIRT1), a deacetylase participating in a broad range of transcriptional and metabolic regulations, may impact cell proliferation and inflammatory responses. However, the role of SIRT1 in RA-FLS was unclear. Here, we explored the effects of SIRT1 on the aggressiveness and inflammatory responses of cultured RA-FLS. SIRT1 expression was significantly lower in synovial tissues and FLS from RA patients than from healthy controls. Overexpression of SIRT1 significantly inhibited RA-FLS proliferation, migration, and invasion. SIRT1 overexpression also significantly increased RA-FLS apoptosis and caspase-3 and -8 activity. Focusing on inflammatory phenotypes, we found SIRT1 significantly reduced RA-FLS secretion of TNF-α, IL-6, IL-8, and IL-1β. Mechanistic studies further revealed SIRT1 suppressed NF-κB pathway by reducing p65 protein expression, phosphorylation, and acetylation in RA-FLS. Our results suggest SIRT1 is a key regulator in RA pathogenesis by suppressing aggressive phenotypes and inflammatory response of FLS. Enhancing SIRT1 expression or function in FLS could be therapeutic beneficial for RA by inhibiting synovial hyperplasia and inflammation.

Indexed as

AdultAgedApoptosisArthritis, RheumatoidArthroplasty, ReplacementCase-Control StudiesCaspase 3Caspase 8Cell CycleCell MovementCell ProliferationFemaleGene Expression RegulationHumansInterleukin-1betaInterleukin-6CASP3 protein, humanCASP8 protein, humanCaspase 3Caspase 8IL1B protein, humanIL6 protein, humanInterleukin-1betaInterleukin-6Interleukin-8SIRT1 protein, humanSirtuin 1Transcription Factor RelATumor Necrosis Factor-alphafibroblast-like synoviocytesinflammationNF-κBrheumatoid arthritissirtuin 1

Identifiers

PMID29784872
PMCPMC6013706
OpenAlexW2803558798

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.