Evidence map›Paper›PMID 30972153›Full record

ReviewAmerican journal of translational research2019

Interleukin-27 prevents LPS-induced inflammatory osteolysis by inhibiting osteoclast formation and function.

Xianghe Li, Wei Luo, Junxian Hu, Yueqi Chen, Tao Yu, Jing Yang, Shiwu Dong, Xiaobin Tian, Li Sun

Open access · greenAbstract readReview
In one paragraph

Review in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  3. The Role of Cytokines in Orthodontic Tooth Movement.International journal of molecular sciences · 2025
    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

9 authors at 3 institutions in 1 country.

Xianghe LiGuizhou Medical University Guiyang 550025, China.
Wei LuoGuizhou Medical University Guiyang 550025, China.
Junxian HuDepartment of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University) Chongqing 400038, China.
Yueqi ChenDepartment of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University) Chongqing 400038, China.
Tao YuDepartment of Orthopedics, Southwest Hospital, Third Military Medical University (Army Medical University) Chongqing 400038, China.
Jing YangCenter of Trauma of Daping Hospital, Third Military Medical University (Army Medical University) Chongqing 400038, China.
Shiwu DongDepartment of Biomedical Materials Science, Third Military Medical University (Army Medical University) Chongqing 400038, China.
Xiaobin TianGuizhou Medical University Guiyang 550025, China.
Li SunDepartment of Orthopedics, Guizhou Province People's Hospital Guiyang 550002, China.
Army Medical University · CNGuiyang Medical University · CNGuizhou Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteolysis is a serious complication of several chronic inflammatory diseases and is closely associated with a local chronic inflammatory reaction with a variety of causes. Inflammatory factors and osteoclastogenesis can enhance bone erosion. Interleukin-27 (IL-27) is speculated to play an important role in the physiological immune response. However, there are few studies on its effects on osteoclastogenesis. In this study, IL-27 was shown to inhibit receptor activator nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis. The gene expression levels of osteoclast (OC)-specific genes, such as nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and C-FOS, which are essential for OC differentiation and bone resorption, were significantly reduced. Further investigating the underlying mechanism, we found that IL-27 significantly reduced RANKL-induced osteoclastogenesis by inhibiting the phosphorylation of IκB and phosphorylation of nuclear factor κB (NF-κB) p65. Furthermore, IL-27 was shown to inhibit lipopolysaccharide (LPS)-induced osteolysis in vivo. Collectively, these results indicate that IL-27 may be a potential candidate for the treatment of osteolytic diseases.

Indexed as

inflammatory osteolysisInterleukin-27lipopolysaccharideosteoclast

Identifiers

PMID30972153
PMCPMC6456512
OpenAlexW2990577530

What OpenQuestion holds

Textmetadata
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.