Evidence map›Paper›PMID 32251998›Full record

ArticleEBioMedicine2020

Targeted apoptosis of myofibroblasts by elesclomol inhibits hypertrophic scar formation.

Yi Feng, Jun-Jie Wu, Zi-Li Sun, Si-Yu Liu, Ming-Li Zou, Zheng-Dong Yuan, Shun Yu, Guo-Zhong Lv, Feng-Lai Yuan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 2 pooled it
6.6field-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

47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  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

9 authors at 4 institutions in 1 country.

Yi FengDepartment of Burns and Plastic Surgery, The Affiliated Hospital of Jiangnan University, Wuxi 214041, China; Department of Pharmacology, Medical School, Yangzhou University, Yangzhou 225001, China.
Jun-Jie WuDepartment of Burns and Plastic Surgery, The Affiliated Hospital of Jiangnan University, Wuxi 214041, China.
Zi-Li SunDepartment of Burns and Plastic Surgery, The Affiliated Hospital of Jiangnan University, Wuxi 214041, China; Wuxi Clinical Medicine School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Wuxi 214041, China.
Si-Yu LiuDepartment of Burns and Plastic Surgery, The Affiliated Hospital of Jiangnan University, Wuxi 214041, China; Wuxi Clinical Medicine School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Wuxi 214041, China.
Ming-Li ZouDepartment of Burns and Plastic Surgery, The Affiliated Hospital of Jiangnan University, Wuxi 214041, China; Wuxi Clinical Medicine School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Wuxi 214041, China.
Zheng-Dong YuanDepartment of Burns and Plastic Surgery, The Affiliated Hospital of Jiangnan University, Wuxi 214041, China.
Shun YuDepartment of Burns and Plastic Surgery, The Affiliated Hospital of Jiangnan University, Wuxi 214041, China; Wuxi Clinical Medicine School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Wuxi 214041, China; Department of Central Laboratory, The Third Hospital Affiliated to Nantong University, Wuxi, Jiangsu 214041, China.
Guo-Zhong LvDepartment of Burns and Plastic Surgery, The Affiliated Hospital of Jiangnan University, Wuxi 214041, China; Wuxi Clinical Medicine School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Wuxi 214041, China; Department of Central Laboratory, The Third Hospital Affiliated to Nantong University, Wuxi, Jiangsu 214041, China; Engineering Research Center of the Ministry of Education for Wound Repair Technology, Jiangnan University, Wuxi 214041, China.
Feng-Lai YuanDepartment of Burns and Plastic Surgery, The Affiliated Hospital of Jiangnan University, Wuxi 214041, China; Wuxi Clinical Medicine School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Wuxi 214041, China; Department of Central Laboratory, The Third Hospital Affiliated to Nantong University, Wuxi, Jiangsu 214041, China; Engineering Research Center of the Ministry of Education for Wound Repair Technology, Jiangnan University, Wuxi 214041, China. Electronic address: bjjq88@163.com.
Wuxi Fourth People's Hospital · CNJiangnan University · CNNanjing University of Chinese Medicine · CNWuxi Third People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypertrophic scar (HS) is characterized by the increased proliferation and decreased apoptosis of myofibroblasts. Myofibroblasts, the main effector cells for dermal fibrosis, develop from normal fibroblasts. Thus, the stimulation of myofibroblast apoptosis is a possible treatment for HS. We aimed to explore that whether over-activated myofibroblasts can be targeted for apoptosis by anticancer drug elesclomol.

methods4',6-diamidino-2-phenylindole staining, flow cytometry, western blotting, collagen gel contraction and immunofluorescence assays were applied to demonstrate the proapoptotic effect of elesclomol in scar derived myofibroblasts and TGF-β1 induced myofibroblasts. The therapeutic potential of elesclomol was investigated by establishing rabbit ear hypertrophic scar models.

findingsBoth 4',6-diamidino-2-phenylindole staining and flow cytometry indicated that elesclomol targets myofibroblasts in vitro. Collagen gel contraction assay showed that elesclomol inhibited myofibroblast contractility. Flow cytometry and western blot analysis revealed that elesclomol resulted in excessive intracellular levels of reactive oxygen species(ROS), and caspase-3 and cytochrome c proteins. Moreover, compared with the control group, the elesclomol group had a significantly lower scar elevation index in vivo. Immunofluorescence assays for TUNEL and α-smooth muscle actin indicated that elesclomol treatment increased the number of apoptotic myofibroblasts.

interpretationThe above results indicate that elesclomol exerted a significant inhibitory effect on HS formation via targeted myofibroblast apoptosis associated with increased oxidative stress. Thus, elesclomol is a promising candidate drug for the treatment of myofibroblast-related diseases such as HS.

Indexed as

ApoptosisAdolescentAdultCaspase 3CicatrixFemaleHumansHydrazinesMaleMyofibroblastsReactive Oxygen SpeciesCaspase 3elesclomolHydrazinesReactive Oxygen SpeciesApoptosisElesclomolHypertrophic scarMyofibroblastsROS

Identifiers

PMID32251998
PMCPMC7132150
OpenAlexW3015143081

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.