Evidence map›Paper›PMID 29849053›Full record

ArticleScientific reports2018

Profibrogenic effect of high-mobility group box protein-1 in human dermal fibroblasts and its excess in keloid tissues.

Won Jai Lee, Seung Yong Song, Hyun Roh, Hyo Min Ahn, Youjin Na, Jihee Kim, Ju Hee Lee, Chae Ok Yun

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  6. Article
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  8. Article
  9. Article
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  11. Fibrosis in burns: an overview of mechanisms and therapies.American journal of physiology. Cell physiology · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. Article
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

8 authors at 2 institutions in 1 country.

Won Jai LeeInstitute for Human Tissue Restoration, Department of Plastic & Reconstructive Surgery, Yonsei University College of Medicine, Seoul, Korea.
Seung Yong SongInstitute for Human Tissue Restoration, Department of Plastic & Reconstructive Surgery, Yonsei University College of Medicine, Seoul, Korea.
Hyun RohInstitute for Human Tissue Restoration, Department of Plastic & Reconstructive Surgery, Yonsei University College of Medicine, Seoul, Korea.
Hyo Min AhnDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul, Korea.
Youjin NaDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul, Korea.
Jihee KimDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Ju Hee LeeDepartment of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea. juhee@yuhs.ac.
Chae Ok YunDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul, Korea. chaeok@hanyang.ac.krs.
Yonsei University · KRHanyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-mobility group box 1 (HMGB1) protein acts as a DNA chaperone for nuclear homeostasis. It translocates into the cytosol and is secreted into extracellular spaces, triggering proinflammatory cytokines and acting as a mediator in fibrosis. We determined whether HMGB1 plays a role in normal dermal fibrosis and keloid, and is involved with transforming growth factor β. We investigated the translocation and active release of HMGB1 from normal dermal fibroblasts under lipopolysaccharide stimuli, and the redistribution of nuclear HMGB1 into the cytoplasm of keloid fibroblasts. HMGB1 and its effector toll-like receptors and receptors for advanced glycation end product proteins are actively expressed in keloid tissues. Exogenous HMGB1 can induce the proliferation of human dermal fibroblasts, and could act as a profibrogenic molecule to produce collagen, decrease MMP-1, and increase TIMP-1 mRNA expression. Moreover, administration of HMGB1 increased the expression level of TGF-β1 and internal signaling molecules, such as Smad 2 and 3, phosphorylated Smad 2/3 complex, Erk 1/2, Akt, and NF-κB. Collectively, we demonstrate that HMGB1 treatment increases the expression level of collagen types I and III, elastin, and fibronectin in dermal spheroid cultures, thus making HMGB1 a promising therapeutic target for treatment of profibrogenic diseases.

Indexed as

FibroblastsGene Expression Regulation, EnzymologicHMGB1 ProteinHumansIntracellular SpaceKeloidMatrix Metalloproteinase 1Matrix Metalloproteinase 2Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa BProto-Oncogene Proteins c-aktSignal TransductionSkinTissue Inhibitor of Metalloproteinase-1Transforming Growth Factor beta1HMGB1 ProteinMatrix Metalloproteinase 1Matrix Metalloproteinase 2Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa BProto-Oncogene Proteins c-aktTissue Inhibitor of Metalloproteinase-1Transforming Growth Factor beta1

Identifiers

PMID29849053
PMCPMC5976629
OpenAlexW2806323543

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.