Evidence map›Paper›PMID 27176130›Full record

ArticleMolecular medicine reports2016

CLI-095 decreases atherosclerosis by modulating foam cell formation in apolipoprotein E-deficient mice.

Xiao-Qing Wang, Hui-Qing Wan, Xian-Jing Wei, Ying Zhang, Peng Qu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 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
1.1field-weighted citation impact, top 23% 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, 17 citations in OpenAlex.

  1. Review
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  5. Vasculoprotective Effects of Vildagliptin. Focus on Atherogenesis.International journal of molecular sciences · 2020
    Review
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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 4 institutions in 1 country.

Xiao-Qing WangDepartment of Cardiology, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116023, P.R. China.
Hui-Qing WanDepartment of Pharmacy, Dongguan People's Hospital, Dongguan, Guangdong 523000, P.R. China.
Xian-Jing WeiDepartment of Cardiology, Affiliated Zhongshan Hospital of Dalian University, Dalian, Liaoning 116023, P.R. China.
Ying ZhangDepartment of Cardiology, Affiliated Zhongshan Hospital of Dalian University, Dalian, Liaoning 116023, P.R. China.
Peng QuDepartment of Cardiology, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116023, P.R. China.
Affiliated Zhongshan Hospital of Dalian University · CNDalian Medical University · CNDongguan People’s Hospital · CNSecond Affiliated Hospital of Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptor 4 (TLR4) is considered to have a critical role in the occurrence and development of atherosclerosis in atherosclerosis-prone mice; however, it remains uncertain whether treatment with a TLR4 inhibitor may attenuate atherosclerosis. The present study aimed to determine the vascular protective effects of the TLR4 inhibitor CLI-095 on apolipoprotein E‑deficient (ApoE‑/‑) mice. ApoE‑/‑ mice were fed either chow or a high‑fat diet, and were treated with or without CLI‑095 for 10 weeks. The mean atherosclerotic plaque area in the aortic sections of CLI‑095‑treated mice was 54.3% smaller than in the vehicle‑treated mice (P=0.0051). In vitro, murine peritoneal macrophages were treated with or without CLI‑095, and were subsequently stimulated with oxidized low‑density lipoprotein. Treatment with CLI‑095 markedly reduced the expression levels of lectin‑like oxidized low‑density lipoprotein receptor‑1 and acyl-coenzyme A:cholesterol acyltransferase‑1, and significantly upregulated the expression levels of ATP‑binding cassette transporter A1, predominantly via suppressing activation of the TLR4/nuclear factor‑κB signaling pathway. The results of the present study indicated that the TLR4 inhibitor CLI‑095 has the ability to suppress the progression of atherosclerosis in an in vivo model by reducing macrophage foam cell formation.

Indexed as

AnimalsApolipoproteins EAtherosclerosisATP Binding Cassette Transporter 1BiomarkersDisease Models, AnimalFoam CellsGene ExpressionImmunohistochemistryLipidsMacrophagesMacrophages, PeritonealMaleMiceMice, KnockoutPlaque, AtheroscleroticApolipoproteins EATP Binding Cassette Transporter 1Biomarkersethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylateLipidsSterol O-Acyltransferasesterol O-acyltransferase 1SulfonamidesToll-Like Receptor 4

Identifiers

PMID27176130
PMCPMC4918599
OpenAlexW2387073006

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.