Evidence map›Paper›PMID 30463229›Full record

ArticleInternational journal of molecular sciences2018

Visfatin Promotes Wound Healing through the Activation of ERK1/2 and JNK1/2 Pathway.

Byung-Cheol Lee, Jisun Song, Arim Lee, Daeho Cho, Tae Sung Kim

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. Heliyon · 2024
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. The Role of Adipokines in Inflammatory Mechanisms of Obesity.International journal of molecular sciences · 2022
    Review
  8. Review
  9. iScience · 2022
    Article
  10. Biomimetics (Basel, Switzerland) · 2022
    Article
  11. Review
  12. Review
  13. Article
  14. Adipokines in the Skin and in Dermatological Diseases.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Article
  17. 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

5 authors.

Byung-Cheol LeeDepartment of Life Sciences, College of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Korea. microlbc@korea.ac.kr.ORCID 0000-0001-5163-3586
Jisun SongDepartment of Life Sciences, College of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Korea. wltjs529@hanmail.net.
Arim LeeDepartment of Life Sciences, College of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Korea. arim323@korea.ac.kr.
Daeho ChoInstitute of Convergence Science, Korea University, Seoul 136-701, Korea. cdhkor@korea.ac.kr.
Tae Sung KimDepartment of Life Sciences, College of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Korea. tskim@korea.ac.kr.

Funding

The Creative Materials Discovery Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science ICT and Future Planning 2016M3D1A1021387
6 · The paper itself

Abstract

Visfatin, a member of the adipokine family, plays an important role in many metabolic and stress responses. The mechanisms underlying the direct therapeutic effects of visfatin on wound healing have not been reported yet. In this study, we examined the effects of visfatin on wound healing in vitro and in vivo. Visfatin enhanced the proliferation and migration of human dermal fibroblasts (HDFs) and keratinocytes the expression of wound healing-related vascular endothelial growth factor (VEGF) in vitro and in vivo. Treatment of HDFs with visfatin induced activation of both extracellular signal-regulated kinases 1 and 2 (ERK1/2) and c-Jun N-terminal kinases 1 and 2 (JNK1/2) in a time-dependent manner. Inhibition of ERK1/2 and JNK1/2 led to a significant decrease in visfatin-induced proliferation and migration of HDFs. Importantly, blocking VEGF with its neutralizing antibodies suppressed the visfatin-induced proliferation and migration of HDFs and human keratinocytes, indicating that visfatin induces the proliferation and migration of HDFs and human keratinocytes via increased VEGF expression. Moreover, visfatin effectively improved wound repair in vivo, which was comparable to the wound healing activity of epidermal growth factor (EGF). Taken together, we demonstrate that visfatin promotes the proliferation and migration of HDFs and human keratinocytes by inducing VEGF expression and can be used as a potential novel therapeutic agent for wound healing.

Indexed as

AnimalsCell MovementCell ProliferationCytokinesDermisFibroblastsHumansKeratinocytesMAP Kinase Signaling SystemMice, Inbred BALB CNicotinamide PhosphoribosyltransferaseVascular Endothelial Growth Factor AWound HealingCytokinesNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, humanVascular Endothelial Growth Factor AMAPKVEGFvisfatinwound healing

Identifiers

PMID30463229
PMCPMC6274809

What Socratic 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 Socratic graph.