Evidence map›Paper›PMID 35082796›Full record

ArticleFrontiers in immunology2021

The Polygenic Map of Keloid Fibroblasts Reveals Fibrosis-Associated Gene Alterations in Inflammation and Immune Responses.

Yang Li, Min Li, Caijie Qu, Yongxi Li, Zhanli Tang, Zhike Zhou, Zengzhao Yu, Xu Wang, Linlin Xin, Tongxin Shi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. The role of IL-17 and Th17 cells in keloid pathogenesis.Archives of dermatological research · 2024
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  19. Characterization of the skin keloid microenvironment.Cell communication and signaling : CCS · 2023
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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 4 institutions in 1 country.

Yang LiDepartment of Dermatology, The Affiliated Qingdao Municipal Hospital of Qingdao University, Qingdao, China.
Min LiDepartment of Dermatology, The Affiliated Qingdao Municipal Hospital of Qingdao University, Qingdao, China.
Caijie QuDepartment of Dermatology, The Affiliated Qingdao Municipal Hospital of Qingdao University, Qingdao, China.
Yongxi LiDepartment of Dermatology, The Affiliated Qingdao Municipal Hospital of Qingdao University, Qingdao, China.
Zhanli TangDepartment of Dermatology, Qilu Hospital, Shandong University, Jinan, China.
Zhike ZhouDepartment of Dermatology, The Affiliated Qingdao Municipal Hospital of Qingdao University, Qingdao, China.
Zengzhao YuDepartment of Dermatology, The Affiliated Qingdao Municipal Hospital of Qingdao University, Qingdao, China.
Xu WangDepartment of Dermatology, The Affiliated Qingdao Municipal Hospital of Qingdao University, Qingdao, China.
Linlin XinDepartment of Dermatology, Shandong Provincial Qianfoshan Hospital, The First Hospital Affiliated with Shandong First Medical University, Jinan, China.
Tongxin ShiDepartment of Dermatology, The Affiliated Qingdao Municipal Hospital of Qingdao University, Qingdao, China.
Qingdao Municipal Hospital · CNQingdao University · CNQilu Hospital of Shandong University · CNShandong Provincial QianFoShan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Due to many inconsistencies in differentially expressed genes (DEGs) related to genomic expression changes during keloid formation and a lack of satisfactory prevention and treatment methods for this disease, the critical biomarkers related to inflammation and the immune response affecting keloid formation should be systematically clarified. Normal skin/keloid scar tissue-derived fibroblast genome expression data sets were obtained from the Gene Expression Omnibus (GEO) and ArrayExpress databases. Hub genes have a high degree of connectivity and gene function aggregation in the integration network. The hub DEGs were screened by gene-related protein-protein interactions (PPIs), and their biological processes and signaling pathways were annotated to identify critical biomarkers. Finally, eighty-one hub DEGs were selected for further analysis, and some noteworthy signaling pathways and genes were found to be closely related to keloid fibrosis. For example, IL17RA is involved in IL-17 signal transduction, TIMP2 and MMP14 activate extracellular matrix metalloproteinases, and TNC, ITGB2, and ITGA4 interact with cell surface integrins. Furthermore, changes in local immune cell activity in keloid tissue were detected by DEG expression, immune cell infiltration, and mass CyTOF analyses. The results showed that CD4+ T cells, CD8+ T cells and NK cells were abnormal in keloid tissue compared with normal skin tissue. These findings not only support the key roles of fibrosis-related pathways, immune cells and critical genes in the pathogenesis of keloids but also expand our understanding of targets that may be useful for the treatment of fibrotic diseases.

Indexed as

Disease SusceptibilityImmunityComputational BiologyFibroblastsFibrosisGene Expression ProfilingGene Expression RegulationGene OntologyGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansInflammationKeloidProtein Interaction MappingProtein Interaction MapsSignal Transductionfibroblastsgenome-wide expressionimmune responseinflammationkeloidmolecular alterations

Identifiers

PMID35082796
PMCPMC8785650
OpenAlexW4206113910

What OpenQuestion holds

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LicenceCC BY
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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.