Evidence map›Paper›PMID 28054407›Full record

ReviewCell proliferation2017

From genetics to epigenetics: new insights into keloid scarring.

Yongjing He, Zhenjun Deng, Mansour Alghamdi, Lechun Lu, Mark W Fear, Li He

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell proliferation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
7.3field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Identification of Epigenetic Regulator-Associated Genes in Keloid Disease Through Integrated Bulk and Single-Cell Transcriptomics With RT-qPCR Validation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Characterization of the skin keloid microenvironment.Cell communication and signaling : CCS · 2023
    Review
  12. The Role of Physical Therapies in Wound Healing and Assisted Scarring.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Loureirin A Exerts Antikeloid Activity by Antagonizing the TGF-Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  19. Review
  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

6 authors at 3 institutions in 3 countries.

Yongjing HeDepartment of Plastic Surgery, Second Affiliated Hospital of Kunming Medical University, Kunming, China.
Zhenjun DengDepartment of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming, China.
Mansour AlghamdiBurn Injury Research Unit, School of Surgery, University of Western Australia, Crawley, WA, Australia.
Lechun LuDepartment of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming, China.
Mark W FearBurn Injury Research Unit, School of Surgery, University of Western Australia, Crawley, WA, Australia.
Li HeDepartment of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming, China.
First Affiliated Hospital of Kunming Medical University · CNKunming Medical University · CNUniversity of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Keloid scarring is a dermal fibroproliferative response characterized by excessive and progressive deposition of collagen; aetiology and molecular pathology underlying keloid formation and progression remain unclear. Genetic predisposition is important in the pathogenic processes of keloid formation, however, environmental factors and epigenetic mechanisms may also play pivotal roles. Epigenetic modification is a recent area of investigation in understanding the molecular pathogenesis of keloid scarring and there is increasing evidence that epigenetic changes may play a role in induction and persistent activation of fibroblasts in keloid scars. Here we have reviewed three epigenetic mechanisms: DNA methylation, histone modification and the role of non-coding RNAs. We also review the evidence that these mechanisms may play a role in keloid formation - in future, it may be possible that epigenetic markers may be used instead of prognostic or diagnostic markers here. However, there is a significant amount of work required to increase our current understanding of the role of epigenetic modification in keloid disease.

Indexed as

AnimalsCells, CulturedCollagenDNA MethylationEpigenesis, GeneticFibroblastsHumansKeloidCollagen

Identifiers

PMID28054407
PMCPMC6529126
OpenAlexW2571501940

What OpenQuestion holds

Textmetadata
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.