Evidence map›Paper›PMID 26848572›Full record

ArticlePloS one2016

Visfatin Destabilizes Atherosclerotic Plaques in Apolipoprotein E-Deficient Mice.

Bo Li, Yunhe Zhao, Hui Liu, Bin Meng, Jitao Wang, Tianjun Qi, Hui Zhang, Tao Li, Peiqing Zhao, Hui Sun and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 26 citations in OpenAlex.

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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

14 authors at 4 institutions in 1 country.

Bo LiDepartment of Cardiology, Central Hospital of Zibo, Zibo, PR China.
Yunhe ZhaoDepartment of Cardiology, Central Hospital of Zibo, Zibo, PR China.
Hui LiuDepartment of Cardiology, Qilu Hospital of Shandong University, Ji'nan, PR China.
Bin MengDepartment of Cardiology, Central Hospital of Zibo, Zibo, PR China.
Jitao WangDepartment of Cardiology, Central Hospital of Zibo, Zibo, PR China.
Tianjun QiDepartment of Cardiology, Central Hospital of Zibo, Zibo, PR China.
Hui ZhangDepartment of Cardiology, Central Hospital of Zibo, Zibo, PR China.
Tao LiDepartment of Cardiology, Central Hospital of Zibo, Zibo, PR China.
Peiqing ZhaoDepartment of Cardiology, Central Hospital of Zibo, Zibo, PR China.
Hui SunDepartment of Cardiology, Central Hospital of Zibo, Zibo, PR China.
Jia XuPrenatal Diagnosis Center, Zibo Maternal and Child Health Hospital, Zibo, PR China.
Haibo SongPrenatal Diagnosis Center, Zibo Maternal and Child Health Hospital, Zibo, PR China.
Zhe DongDepartment of Cardiology, China-Japan Friendship Hospital, Chaoyang District, Beijing, China.
Fengshuang AnDepartment of Cardiology, Qilu Hospital of Shandong University, Ji'nan, PR China.
Central Hospital of Zibo · CNQilu Hospital of Shandong University · CNThe Fourth People's Hospital of Zibo City · CNChina-Japan Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesAlthough there is evidence that visfatin is associated with atherogenesis, the effect of visfatin on plaque stability has not yet been explored.

methodsIn vivo, vulnerable plaques were established by carotid collar placement in apolipoprotein E-deficient (ApoE-/-) mice, and lentivirus expressing visfatin (lenti-visfatin) was locally infused in the carotid artery. The lipid, macrophage, smooth muscle cell (SMC) and collagen levels were evaluated, and the vulnerability index was calculated. In vitro, RAW264.7 cells were stimulated with visfatin, and the MMPs expressions were assessed by western blot and immunofluorescence. And the mechanism that involved in visfatin-induced MMP-8 production was investigated.

resultsTransfection with lenti-visfatin significantly promoted the expression of visfatin which mainly expressed in macrophages in the plaque. Lenti-visfatin transfection significantly promoted the accumulation of lipids and macrophages, modulated the phenotypes of smooth muscle cells and decreased the collagen levels in the plaques, which significantly decreased the plaque stability. Simultaneously, transfection with lenti-visfatin significantly up-regulated the expression of MMP-8 in vivo, as well as MMP-1, MMP-2 and MMP-9. Recombinant visfatin dose- and time-dependently up-regulated the in vitro expression of MMP-8 in macrophages. Visfatin promoted the translocation of NF-κB, and inhibition of NF-κB significantly reduced visfatin-induced MMP-8 production.

conclusionsVisfatin increased MMP-8 expression, promoted collagen degradation and increased the plaques vulnerability index.

Indexed as

AnimalsApolipoproteins EAtherosclerosisCell LineCollagenCytokinesLentivirusLipidsMacrophagesMaleMatrix Metalloproteinase 13Matrix Metalloproteinase 2Matrix Metalloproteinase 8Matrix Metalloproteinase 9MiceMice, KnockoutApolipoproteins ECollagenCytokinesLipidsMatrix Metalloproteinase 13Matrix Metalloproteinase 2Matrix Metalloproteinase 8Matrix Metalloproteinase 9Mmp13 protein, mouseMmp2 protein, mouseMMP8 protein, mouseMmp9 protein, mouseNF-kappa BNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, mouse

Identifiers

PMID26848572
PMCPMC4743838
OpenAlexW2255838500

What OpenQuestion holds

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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.