Evidence map›Paper›PMID 37021598›Full record

ArticleActa dermato-venereologica2023

Dasatinib Attenuates Fibrosis in Keloids by Decreasing Senescent Cell Burden.

Claudia C Darmawan, Keunyoung Hur, Novi Kusumaningrum, Jin Ho Chung, Si-Hyung Lee, Je-Ho Mun

Open access · goldAbstract read
In one paragraph

Article in Acta dermato-venereologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Observational
  5. Review
  6. Review
  7. Review
  8. Article
  9. 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 2 countries.

Claudia C DarmawanDepartment of Dermatology, Seoul National University College of Medicine, Seoul, Korea; Institute of Human-Environment Interface Biology, Seoul National University, Seoul, Korea.
Keunyoung HurDepartment of Dermatology, Seoul National University College of Medicine, Seoul, Korea; Institute of Human-Environment Interface Biology, Seoul National University, Seoul, Korea; Department of Dermatology, Seoul National University Hospital, Seoul, Korea.
Novi KusumaningrumDepartment of Dermatology, Seoul National University College of Medicine, Seoul, Korea; Institute of Human-Environment Interface Biology, Seoul National University, Seoul, Korea.
Jin Ho ChungDepartment of Dermatology, Seoul National University College of Medicine, Seoul, Korea; Institute of Human-Environment Interface Biology, Seoul National University, Seoul, Korea; Department of Dermatology, Seoul National University Hospital, Seoul, Korea.
Si-Hyung LeeDepartment of Dermatology, Seoul National University College of Medicine, Seoul, Korea; Institute of Human-Environment Interface Biology, Seoul National University, Seoul, Korea; Department of Dermatology, Seoul National University Hospital, Seoul, Korea. always5515@gmail.com.
Je-Ho MunDepartment of Dermatology, Seoul National University College of Medicine, Seoul, Korea; Institute of Human-Environment Interface Biology, Seoul National University, Seoul, Korea; Department of Dermatology, Seoul National University Hospital, Seoul, Korea. jehomun@gmail.com.
Seoul National University Hospital · KRSeoul National University · KRNew Generation University College · ET

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Keloids are skin tumours caused by aberrant growth of dermal fibroblasts. Cellular senescence contributes to aging and various pathological conditions, including cancer, atherosclerosis, and fibrotic diseases. However, the effects of cellular senescence and senolytic drugs on keloids remain largely unknown. This study investigated senescent fibroblasts in keloids and assessed the effects of dasatinib on these cells. Tissues acquired from keloid removal surgery were analysed for senescence-associated β-galactosidase-positive cells, p16 expression, and the effects of dasatinib treatment on keloids. Keloid tissue was xenotransplanted into mice, and the effect of intralesional dasatinib injection on keloid growth was observed. The results showed that the numbers of β-galactosidase-positive and p16-expressing cells were higher in the keloids compared with in the controls. Dasatinib induced selective clearance of senescent cells and decreased procollagen expression in cultured keloid fibroblasts. In this xenotransplant keloid mouse model, intralesional injection of dasatinib reduced gross keloid tissue weight and the expression of both procollagen and p16. In addition, dasatinib-treated keloid fibroblasts conditioned medium reduced procollagen and p16 expression in cultured keloid fibroblasts. In conclusion, these results suggest that an increased number of senescent fibroblasts may play an important role in the pathogenesis of keloids. Therefore, dasatinib could be an alternative treatment for patients with keloids.

Indexed as

KeloidAnimalsCells, CulturedCellular SenescenceDasatinibFibroblastsMiceProcollagenDasatinibProcollagen

Identifiers

PMID37021598
PMCPMC10108619
OpenAlexW4362657067

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.