Evidence map›Paper›PMID 27695484›Full record

ArticleArchives of medical science : AMS2016

NLRP3 inflammasome: a novel link between lipoproteins and atherosclerosis.

Wang Li Li, Li Gui Hua, Peng Qu, Wang Hong Yan, Cui Ming, Yuan Da Jun, Lou Da Yuan, Niu Nan

Open access · goldAbstract read
In one paragraph

Article in Archives of medical science : AMS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 34 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

8 authors at 2 institutions in 1 country.

Wang Li LiDepartment of Cardiology, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Li Gui HuaDepartment of Cardiology, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Peng QuDepartment of Cardiology, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Wang Hong YanDepartment of Cardiology, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Cui MingDepartment of Emergency, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Yuan Da JunDepartment of Cardiology, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Lou Da YuanDepartment of Cardiology, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Niu NanDepartment of Cardiology, Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Second Affiliated Hospital of Dalian Medical University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPattern recognition receptor-mediated signaling pathways have recently been elucidated to bridge the innate immune system and atherosclerosis. NLRP3 is a member of the NLR family. Upon activation, it initiates IL-1β and IL-18 processing, a key step in the inflammatory process of atherosclerosis. MATERIAL AND

methodsWe used three different types of lipoproteins, ox-LDL, ox-HDL, and HDL, in Thp-1 at the concentration of 50 mg/l, 100 mg/l, and 150 mg/l respectively. Using real-time polymerase chain reaction and western blot, ELISA detected the expression of NLRP3 and downstream cytokines. NLRP3 siRNA was constructed to down-regulate expression of the NLRP3 gene via the RNA interference technique. 150 mg/l of ox-LDL, ox-HDL and HDL was added to the Thp-1 cell line respectively. We observed the changes in the expression of caspase-1, IL-1β and IL-18 when the NLRP3 gene was down-regulated.

resultsOx-LDL and ox-HDL addition not only increases the expression of NLRP3, but also activates the NLRP3 downstream cytokines and caspase-1 and induces IL-1β and IL-18 secretion. Moreover, the effects of activation and induction are shown to have a dose-dependent manner. Expression of NLRP3 and its downstream inflammatory cytokines is reduced in the presence of HDL (

conclusionsThe data suggest that activation of the NLRP3 inflammasome is a critical step in caspase-1 activation and IL-1β and IL-18 secretion. Interference with the NLRP3 inflammasome can significantly inhibit the generation of cytokines, thus impeding the pathogenesis of inflammation.

Indexed as

atherosclerosisinflammasomelipoproteinmonocytesNLRP3

Identifiers

PMID27695484
PMCPMC5016581
OpenAlexW2492724695

What OpenQuestion holds

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LicenceCC BY-NC-SA
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Registered trials

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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.