Evidence map›Paper›PMID 30414292›Full record

ArticleJournal of cellular physiology2019

Interleukin-37 inhibits osteoclastogenesis and alleviates inflammatory bone destruction.

Ruohui Tang, Jin Yi, Jing Yang, Yueqi Chen, Wei Luo, Shiwu Dong, Jun Fei

Open access · hybridAbstract read
In one paragraph

Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

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  12. Diallyl disulfide alleviates inflammatory osteolysis by suppressing osteoclastogenesisFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
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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

7 authors at 2 institutions in 1 country.

Ruohui TangCenter of Trauma of Daping Hospital, Third Military Medical University, Chongqing, China.ORCID 0000-0001-6580-3259
Jin YiCenter of Trauma of Daping Hospital, Third Military Medical University, Chongqing, China.
Jing YangCenter of Trauma of Daping Hospital, Third Military Medical University, Chongqing, China.
Yueqi ChenDepartment of Biomedical Materials Science, School of Biomedical Engineering, Third Military Medical University (Army Medical University), Chongqing, China.
Wei LuoDepartment of Osteological, Guizhou Province People's Hospital, Guiyang, China.
Shiwu DongDepartment of Biomedical Materials Science, School of Biomedical Engineering, Third Military Medical University (Army Medical University), Chongqing, China.ORCID 0000-0002-5032-4893
Jun FeiCenter of Trauma of Daping Hospital, Third Military Medical University, Chongqing, China.ORCID 0000-0002-5036-1109
Army Medical University · CNGuizhou Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive osteoclast formation is one of the important pathological features of inflammatory bone destruction. Interleukin-37 (IL-37) is an anti-inflammatory agent that is present throughout the body, but it displays low physiological retention. In our study, high levels of the IL-37 protein were detected in clinical specimens from patients with bone infections. However, the impact of IL-37 on osteoclast formation remains unclear. Next, IL-37 alleviated the inflammatory bone destruction in the mouse in vivo. We used receptor activator of nuclear factor-κB ligand and lipopolysaccharide to trigger osteoclastogenesis under physiological and pathological conditions to observe the role of IL-37 in this process and explore the potential mechanism of this phenomenon. In both induction models, IL-37 exerted inhibitory effects on osteoclast differentiation and bone resorption. Furthermore, IL-37 decreased the phosphorylation of inhibitor of κBα and p65 and the expression of nuclear factor of activated T cells c1, while the dimerization inhibitor of myeloid differentiation factor 88 reversed the effects. These data provide evidence that IL-37 modulates osteoclastogenesis and a theoretical basis for the clinical application of IL-37 as a treatment for bone loss-related diseases.

Indexed as

AnimalsBone and BonesBone ResorptionCell DifferentiationCell LineHumansInflammationInterleukin-1LigandsLipopolysaccharidesMiceMyeloid Differentiation Factor 88NF-kappa BOsteoclastsOsteogenesisRAW 264.7 CellsIL37 protein, humanInterleukin-1LigandsLipopolysaccharidesMyeloid Differentiation Factor 88NF-kappa Binflammatory bone destructioninterleukin-37lipopolysaccharidenuclear factor-κB signalingosteoclast differentiation

Identifiers

PMID30414292
PMCPMC6587950
OpenAlexW2900372706

What OpenQuestion holds

Textmetadata
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.