Evidence map›Paper›PMID 25741130›Full record

ArticleMediators of inflammation2015

Lipid peroxidation-mediated inflammation promotes cell apoptosis through activation of NF-κB pathway in rheumatoid arthritis synovial cells.

Geng Yin, Ying Wang, Xiao-Min Cen, Min Yang, Yan Liang, Qi-Bing Xie

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
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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

6 authors at 2 institutions in 1 country.

Geng YinDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China.
Ying WangDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China.
Xiao-Min CenDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China.
Min YangDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China.
Yan LiangDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China.
Qi-Bing XieDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, China.
Sichuan University · CNWest China Hospital of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation of multiple joints. The central pathogenesis of RA is the proliferation of synovial fibroblasts in response to inflammatory cytokines. However, some of the targeted therapies for inflammation reactions do not display significant clinical improvement after initiation of therapy. Thus, the relationship between inflammatory responses and RA therapy is still incompletely understood. In the present study, we proposed to determine whether enhanced inflammations may lead to cell apoptosis in rheumatoid arthritis synoviocytes. Our results indicated that products of lipid peroxidations, 4-HNE, may induce synovial intrinsic inflammations by activating NF-κB pathways and it may lead to cell apoptosis. Pharmacological inhibition of NF-κB activation may reduce the 4-HNE mediated inflammation responses and subsequent cell apoptosis. Our results may help to clarify the role of inflammations on RA development and imply that blocking NF-κB activation may be partly beneficial for human RA therapy. These findings might provide a mechanism-based rationale for developing new strategy to RA clinical therapy.

Indexed as

Arthritis, RheumatoidCell LineHumansInflammation MediatorsInterleukin-1betaInterleukin-6Lipid PeroxidationNF-kappa BSignal TransductionSynovial MembraneTumor Necrosis Factor-alphaInflammation MediatorsInterleukin-1betaInterleukin-6NF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID25741130
PMCPMC4337269
OpenAlexW1996086875

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.