Evidence map›Paper›PMID 29316707›Full record

ArticleInternational journal of molecular sciences2018

Visfatin Promotes IL-6 and TNF-α Production in Human Synovial Fibroblasts by Repressing miR-199a-5p through ERK, p38 and JNK Signaling Pathways.

Min-Huan Wu, Chun-Hao Tsai, Yuan-Li Huang, Yi-Chin Fong, Chih-Hsin Tang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
6.3field-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

56 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
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  4. CD38 ligation in sepsis promotes nicotinamide phosphoribosyltransferase-mediated IL-6 production in kidney stromal cells.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
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  13. Genetic associations ofInternational journal of medical sciences · 2024
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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

5 authors at 3 institutions in 1 country.

Min-Huan WuPhysical Education Office, Tunghai University, Taichung 40704, Taiwan. mhwu@thu.edu.tw.
Chun-Hao TsaiSchool of Medicine, China Medical University, Taichung 40402, Taiwan. ritsai8615@gmail.com.
Yuan-Li HuangDepartment of Biotechnology, College of Health Science, Asia University, Taichung 41354, Taiwan. yuanli@asia.edu.tw.ORCID 0000-0002-3405-8863
Yi-Chin FongDepartment of Sports Medicine, College of Health Care, China Medical University, Taichung 40402, Taiwan. yichin.fong@msa.hinet.net.
Chih-Hsin TangSchool of Medicine, China Medical University, Taichung 40402, Taiwan. chtang@mail.cmu.edu.tw.ORCID 0000-0002-7113-8352
Asia University · TWChina Medical University · TWTunghai University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA), an inflammatory form of arthritis, is characterized by synovial inflammation and cartilage destruction largely influenced by two key proinflammatory cytokines-interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α). Notably, levels of visfatin (a proinflammatory adipokine) are elevated in patients with OA, although the relationship of visfatin to IL-6 and TNF-α expression in OA pathogenesis has been unclear. In this study, visfatin enhanced the expression of IL-6 and TNF-α in human OA synovial fibroblasts (OASFs) in a concentration-dependent manner and stimulation of OASFs with visfatin promoted phosphorylation of extracellular-signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK), while ERK, p38, and JNK inhibitors or siRNAs all abolished visfatin-induced increases in IL-6 and TNF-α production. Moreover, transfection with miR-199a-5p mimics reversed visfatin-induced increases in IL-6 and TNF-α production. Furthermore, we also found that visfatin-promoted IL-6 and TNF-α production is mediated via the inhibition of miR-199a-5p expression through the ERK, p38, and JNK signaling pathways. Visfatin may therefore be an appropriate target for drug intervention in OA treatment.

Indexed as

MAP Kinase Signaling SystemAgedCells, CulturedFibroblastsHumansInterleukin-6MAP Kinase Kinase 4MicroRNAsMiddle AgedMitogen-Activated Protein Kinase 3Nicotinamide PhosphoribosyltransferaseOsteoarthritisp38 Mitogen-Activated Protein KinasesSynovial FluidTumor Necrosis Factor-alphaInterleukin-6MAP Kinase Kinase 4MicroRNAsmirn199 microRNA, humanMitogen-Activated Protein Kinase 3Nicotinamide Phosphoribosyltransferasep38 Mitogen-Activated Protein KinasesTumor Necrosis Factor-alphaIL-6miR-199a-5posteoarthritisTNF-αvisfatin

Identifiers

PMID29316707
PMCPMC5796139
OpenAlexW2783127674

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.