Evidence map›Paper›PMID 31333955›Full record

ArticlePlastic and reconstructive surgery. Global open2019

Stem Cells in Keloid Lesions: A Review.

Kim H Lim, Tinte Itinteang, Paul F Davis, Swee T Tan

Open access · goldAbstract read
In one paragraph

Article in Plastic and reconstructive surgery. Global open, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Viewing keloids within the immune microenvironment.American journal of translational research · 2022
    Review
  9. Do Mesenchymal Stem Cells Influence Keloid Recurrence?Stem cells and cloning : advances and applications · 2022
    Article
  10. Review
  11. Review
  12. Article
  13. [Correlation study ofZhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021
    Article
  14. Review
  15. Article
  16. The Keloid Disorder: Heterogeneity, Histopathology, Mechanisms and Models.Frontiers in cell and developmental biology · 2020
    Review
  17. Review
  18. Review
  19. 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

4 authors at 2 institutions in 1 country.

Kim H LimGillies McIndoe Research Institute, Wellington, New Zealand.
Tinte ItinteangGillies McIndoe Research Institute, Wellington, New Zealand.
Paul F DavisGillies McIndoe Research Institute, Wellington, New Zealand.
Swee T TanGillies McIndoe Research Institute, Wellington, New Zealand.
Gillies McIndoe Research Institute · NZHutt Hospital · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Keloid disorder (KD) is a fibroproliferative condition caused by dysregulated wound healing following wounding of the skin. The pathogenesis of KD has not been fully elucidated and current treatment is unsatisfactory. There is increasing evidence of the role of stem cells in KD. This review discusses the role of embryonic stem (ESC)-like cells and mesenchymal stem cells in the pathogenesis of KD. It is proposed that dysfunction of the ESC-like population localized to the endothelium of the microvessels and perivascular cells within the keloid-associated lymphoid tissues may give rise to the aberrant fibroblasts and myofibroblasts via a mesenchymal stem cell intermediate in keloid lesions, by undergoing an endothelial-to-mesenchymal transition. We also discuss the role of the renin-angiotensin system (RAS), the immune system, and the inflammatory response, on stem cell proliferation and differentiation. The understanding of the precise roles of these stem cells and interplay of the associated regulatory pathways could lead to the development of targeted therapy for this enigmatic and challenging condition. The demonstration of the expression of components of the RAS and cathepsins B, D, and G that constitute bypass loops of the RAS, by the ESC-like population, suggests that the primitive population may be a therapeutic target by modulation of the RAS, using existing medications.

Identifiers

PMID31333955
PMCPMC6571348
OpenAlexW2945825726

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.