Evidence map›Paper›PMID 29901120›Full record

ArticleMolecular medicine reports2018

Identification of genes and signaling pathways associated with the pathogenesis of juvenile spondyloarthritis.

Zhe Wang, Yudi Han, Zhaoqing Zhang, Cunfeng Jia, Qiang Zhao, Wei Song, Tao Chen, Yifan Zhang, Xiuhui Wang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. Advances in Juvenile Spondyloarthritis.Current rheumatology reports · 2021
    Review
  4. Review
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 5 institutions in 1 country.

Zhe WangDepartment of Orthopedics, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Yudi HanDepartment of Plastic and Reconstructive Surgery, General Hospital of Chinese People's Liberation Army, Beijing 100853, P.R. China.
Zhaoqing ZhangDepartment of Spine Surgery, Zhangqiu People's Hospital, Jinan, Shandong 250200, P.R. China.
Cunfeng JiaDepartment of Spine Surgery, Zhangqiu People's Hospital, Jinan, Shandong 250200, P.R. China.
Qiang ZhaoDepartment of Spine Surgery, Zhangqiu People's Hospital, Jinan, Shandong 250200, P.R. China.
Wei SongSchool of Life Sciences, Shanghai University, Shanghai 200444, P.R. China.
Tao ChenDepartment of Orthopedics, Fourth Hospital of Changsha, Changsha, Hunan 410006, P.R. China.
Yifan ZhangDepartment of Rheumatism Immunity, People's Liberation Army General Hospital, Beijing 100700, P.R. China.
Xiuhui WangDepartment of Orthopedics, Shanghai Zhoupu Hospital, Shanghai 201318, P.R. China.
Zhangqiu City People's Hospital · CNChinese People's Liberation Army · CNFourth Hospital of Changsha · CNShanghai University · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to identify key genes and signaling pathways associated with the pathogenesis of juvenile spondyloarthritis (JSA). The gene expression profile dataset GSE58667, including data from 15 human whole blood samples collected from 11 patients with JSA and four healthy controls, was analyzed to identify differentially expressed genes (DEGs) associated with disease characteristics. Additionally, Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the DEGs were performed. Protein‑protein, microRNA‑transcription factor and chemical‑gene interaction networks were constructed. A total of 326 DEGs, 196 upregulated and 130 downregulated, were identified. DEGs, including C‑X‑C motif chemokine ligand 5 (CXCL5), BCL2 interacting protein 3 like (BNIP3L), dual specificity phosphatase 5 (DUSP5) and tumor protein p53 (TP53) were enriched in functions associated with apoptosis, the cell cycle and immune responses. KEGG pathway enrichment analysis revealed that pathways associated with inflammation and the mitogen‑activated protein kinase 1 (MAPK) signaling pathway were the most enriched by DEGs. The results of the present study indicated that the MAPK signaling pathway and four genes, including CXCL5, BNIP3L, DUSP5 and TP53, may be implicated in the pathogenesis of JSA.

Indexed as

Gene Expression RegulationMAP Kinase Signaling SystemSpondylitis, AnkylosingFemaleHumansMale

Identifiers

PMID29901120
PMCPMC6072139
OpenAlexW2806275512

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.