Evidence map›Paper›PMID 29879032›Full record

ArticleMedicine2018

Inhibition of NF-κB signaling pathway induces apoptosis and suppresses proliferation and angiogenesis of human fibroblast-like synovial cells in rheumatoid arthritis.

Zhong-Bin Xia, Fan-Ru Meng, Yu-Xuan Fang, Xia Wu, Chun-Wang Zhang, Ying Liu, Dan Liu, Guo-Qing Li, Fan-Bo Feng, Hai-Yang Qiu

Open access · goldAbstract read
In one paragraph

Article in Medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. [Puerarin alleviates rheumatoid arthritis in rats by modulating TAK1-mediated TLR4/NF-κB signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  8. Article
  9. Pharmaceuticals (Basel, Switzerland) · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Amelioration of Rheumatoid Arthritis byMedicina (Kaunas, Lithuania) · 2023
    Article
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

10 authors at 3 institutions in 1 country.

Zhong-Bin XiaDepartment of Rheumatology, Clinical Medical College of Yangzhou University (Northern Jiangsu People's Hospital Affiliated to Yangzhou University), Yangzhou Clinical Medical College, Dalian Medical University, Dalian Department of Pathology, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou, PR China.
Fan-Ru Meng
Yu-Xuan Fang
Xia Wu
Chun-Wang Zhang
Ying Liu
Dan Liu
Guo-Qing Li
Fan-Bo Feng
Hai-Yang Qiu
Yangzhou University · CNNorthern Jiangsu People's Hospital · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is the most common inflammatory arthritis and is a major cause of disability. The nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway has been reported to be involved in the pathogenesis of RA with unclear mechanisms. Therefore, this study aims to explore the effect of NF-κB pathway on proliferation, apoptosis, and angiogenesis of human fibroblast-like synovial cells (HFLS) in RA.

methodsNormal HFLS and RA-HFLS were selected as the normal and control groups, respectively. RA-HFLS were treated by BAY11-7082 (an inhibitor of NF-κB) in different concentrations, namely 2.5 μmol/L BAY11-7082, 5 μmol/LBAY11-7082 and 10 μmol/L BAY11-7082. MTT assay was employed to detect cell proliferation. Cell apoptosis was determined by flow cytometry at 24, 48, and 72 hours after culture. Western blot analysis was employed to detect the expressions of NF-κB, angiogenesis-related factors (VEGF, Ang1, and Ang2).

resultsInitially, we found that BAY11-7082 inhibited NF-κB expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-κB), the inhibition of NF-κB pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-dependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner.

conclusionThe study concluded that inhibition of NF-κB pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA.

Indexed as

ApoptosisCell ProliferationNeovascularization, PathologicSignal TransductionArthritis, RheumatoidCells, CulturedHumansMyofibroblastsNF-kappa BNitrilesRibonuclease, PancreaticSulfonesSynoviocytesVascular Endothelial Growth Factor AVesicular Transport Proteins3-(4-methylphenylsulfonyl)-2-propenenitrileangiogeninNF-kappa BNitrilesRibonuclease, PancreaticSulfonesVascular Endothelial Growth Factor AVEGFA protein, humanVesicular Transport ProteinsVPS51 protein, human

Identifiers

PMID29879032
PMCPMC5999456
OpenAlexW2807322906

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.