Evidence map›Paper›PMID 28498809›Full record

ArticleOncotarget2017

Follistatin-like protein 1 promotes inflammatory reactions in nucleus pulposus cells by interacting with the MAPK and NFκB signaling pathways.

Yi Liu, Jianlu Wei, Yunpeng Zhao, Yuanqiang Zhang, Yingguang Han, Bin Chen, Kaiyuan Cheng, Jialin Jia, Lin Nie, Lei Cheng

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

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  16. FSTL1 aggravates OVA-induced inflammatory responses by activating the NLRP3/IL-1β signaling pathway in mice and macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
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  19. Targeting FSTL1 for Multiple Fibrotic and Systemic Autoimmune Diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
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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

10 authors at 2 institutions in 1 country.

Yi LiuDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Jianlu WeiDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Yunpeng ZhaoDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Yuanqiang ZhangDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Yingguang HanDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Bin ChenDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Kaiyuan ChengDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Jialin JiaDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Lin NieDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Lei ChengDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, China.
Qilu Hospital of Shandong University · CNAffiliated Hospital of Shandong Academy of Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveFollistatin-like protein 1 (FSTL1) is a well-known mediator of inflammation. Intervertebral disc disease is an inflammatory disorder. Here, we investigated the role of FSTL1 in the intervertebral discs inflammation.

methodsExpression of FSTL1 in nucleus pulposus tissues from rats and human was determined by immunohistochemistry staining and western blot analysis. The expression levels of tumor necrosis factor-α (TNF-α), interleukin1-β (IL-1β) and matrix metalloproteinase 13 (MMP-13) in human and rat nucleus pulposus tissues were measured by immunohistochemistry staining. The mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NFκB) signaling pathways were detected by western blotting.

resultsFSTL1 serum levels were significantly increased in lumbar disc herniation patients and had a positive correlation with Visual Analogue Scores. Additionally, FSTL1 expression was significantly increased in extrusion group compared with protrusion and control groups. Furthermore, FSTL1 expression was significantly increased in intervertebral disc degeneration models of rats. Immunohistochemistry staining demonstrated that the levels of TNF-α, IL-1β and MMP-13 were increased in the pathogenesis of intervertebral disc disease. Recombinant human FSTL1 significantly increased the production of proinflammatory cytokines in vitro. In addition, FSTL1 promoted inflammation by activating c-Jun N-terminal kinase (JNK), extracellular regulated protein kinases 1/2(ERK1/2) and NFκB signaling.

conclusionsThese data imply that FSTL1 expression was increased in the pathogenesis of intervertebral disc disease. Importantly, FSTL1 promoted inflammatory catabolism in the nucleus pulposus by activating JNK, ERK 1/2/MAPK and NFκB signaling.

Indexed as

Signal TransductionAnimalsBiomarkersCytokinesFemaleFollistatin-Related ProteinsGene ExpressionHumansInflammationInflammation MediatorsIntervertebral Disc DegenerationIntervertebral Disc DisplacementMaleMitogen-Activated Protein KinasesNF-kappa BNucleus PulposusBiomarkersCytokinesFollistatin-Related ProteinsInflammation MediatorsMitogen-Activated Protein KinasesNF-kappa BTumor Necrosis Factor-alphaFSTL1Inflammationlumbar disc herniationMAPK signalingNFκB signaling

Identifiers

PMID28498809
PMCPMC5522124
OpenAlexW2608157571

What OpenQuestion holds

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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.