Evidence map›Paper›PMID 28677720›Full record

ArticleInternational journal of molecular medicine2017

Visfatin induces the apoptosis of endothelial progenitor cells via the induction of pro-inflammatory mediators through the NF-κB pathway.

Lina Sun, Shuchun Chen, Haina Gao, Luping Ren, Guangyao Song

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2017. 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
2.8field-weighted citation impact, top 9% 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.

  1. Pooled it
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  11. The relation of visfatin with nausea and vomiting in the pregnancy.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2020
    Article
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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.

Lina SunDepartment of Endocrinology, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei 06600, P.R. China.
Shuchun ChenDepartment of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
Haina GaoGraduate Student Institute, Hebei Medical University, Shijiazhuang, Hebei 050017, P.R. China.
Luping RenDepartment of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
Guangyao SongDepartment of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
Hebei General Hospital · CNFirst Hospital of Qinhuangdao · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial progenitor cells (EPCs) are an independent factor predicting cardiovascular events. Visfatin plays an important role in the pathogenesis of various metabolic disorders. In this study, we examined the effects of visfatin on the apoptosis of EPCs and the mechanisms underlying these effects. Cultured EPCs pre-treated with various concentrations of visfatin, FK866 (visfatin inhibitor) and BAY11-7085 [referred to as BAY11; nuclear factor-κB (NF-κB) inhibitor] were used to investigate the association between visfatin and EPC apoptosis. Following treatment with visfatin for 48 h, the EPCs exhibited a dose-dependent increase in apoptosis and an upregulated expression of Bax, caspase-3 and NF-κB at both the mRNA and protein level, and a decreased protein expression of Bcl-2. Compared with the untreated control group, the increase in EPC apoptosis, as well as in Bax and caspase-3 expression was significant following treatment with 150 ng/ml visfatin, which also induced a dose-dependent and significant increase in the protein expression of interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1). All the visfatin-induced effects were suppressed by pre-treatment with FK866. Pre-incubation of the EPCs with BAY11 for 1 h followed by treatment with visfatin (150 ng/ml) for 48 h also abolished visfatin-induced apoptosis; it also abolished the promoting effects of visfatin on the expression of caspase-3, Bax, ICAM-1 and IL-6, and its suppressive effects on the protein expression of Bcl-2. On the whole, our data indicate that visfatin induces EPC apoptosis by increasing the expression of pro-inflammatory mediators partly through the regulation of NF-κB.

Indexed as

ApoptosisSignal TransductionAcrylamidesCytokinesEndothelial Progenitor CellsHumansInflammation MediatorsIntercellular Adhesion Molecule-1Interleukin-6NF-kappa BNicotinamide PhosphoribosyltransferaseNitrilesPiperidinesSulfonesAcrylamidesBAY 11-7085CytokinesICAM1 protein, humanIL6 protein, humanInflammation MediatorsIntercellular Adhesion Molecule-1Interleukin-6N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamideNF-kappa BNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, humanNitrilesPiperidinesSulfones

Identifiers

PMID28677720
PMCPMC5547917
OpenAlexW2731451281

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.