Evidence map›Paper›PMID 31552041›Full record

ArticleFrontiers in immunology2019

Formyl Peptide Receptor 2 Activation Ameliorates Dermal Fibrosis and Inflammation in Bleomycin-Induced Scleroderma.

Gyu Tae Park, Yang Woo Kwon, Tae Wook Lee, Seong Gyu Kwon, Hyun-Chang Ko, Moon Bum Kim, Jae Ho Kim

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. WKYMVm Works by Targeting Immune Cells.Journal of inflammation research · 2023
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Therapeutic potential of WKYMVm in diseases.Frontiers in pharmacology · 2022
    Review
  11. Review
  12. SPM Receptor Expression and Localization in Irradiated Salivary Glands.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021
    Article
  13. Article
  14. Article
  15. Review
  16. AFrontiers in pharmacology · 2020
    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

7 authors at 2 institutions in 1 country.

Gyu Tae ParkDepartment of Physiology, Pusan National University School of Medicine, Yangsan-si, South Korea.
Yang Woo KwonDepartment of Physiology, Pusan National University School of Medicine, Yangsan-si, South Korea.
Tae Wook LeeDepartment of Physiology, Pusan National University School of Medicine, Yangsan-si, South Korea.
Seong Gyu KwonDepartment of Physiology, Pusan National University School of Medicine, Yangsan-si, South Korea.
Hyun-Chang KoDepartment of Dermatology, Pusan National University School of Medicine, Yangsan-si, South Korea.
Moon Bum KimDepartment of Dermatology, Pusan National University School of Medicine, Yangsan-si, South Korea.
Jae Ho KimDepartment of Physiology, Pusan National University School of Medicine, Yangsan-si, South Korea.
Pusan National University · KRPusan National University Yangsan Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic sclerosis is a profibrotic autoimmune disease mediated by the dysregulation of extracellular matrix synthesis. Formyl peptide receptor 2 (Fpr2) is a G protein-coupled receptor that modulates inflammation and host defense by regulating the activation of inflammatory cells, such as macrophages. However, the role of Fpr2 in the development and therapy of scleroderma is still unclear. The present study was conducted to investigate the effects of Fpr2 activation in the treatment of scleroderma fibrosis. We found that intradermal administration of WKYMVm, an Fpr2-specific agonist, alleviated bleomycin-induced scleroderma fibrosis in mice and decreased dermal thickness in scleroderma skin. WKYMVm-treated scleroderma skin tissues displayed reduced numbers of myofibroblasts expressing α-smooth muscle actin, Vimentin, and phosphorylated SMAD3. WKYMVm treatment attenuated macrophage infiltration in scleroderma skin and reduced the number of M2 macrophages. The therapeutic effects of WKYMVm in scleroderma-associated fibrosis and inflammation were completely abrogated in Fpr2 knockout mice. Moreover, WKYMVm treatment reduced the serum levels of inflammatory cytokines, such as tumor necrosis factor-α, and interferon-γ, in the scleroderma model of wild-type mice but not in Fpr2 knockout mice. These results suggest that WKYMVm-induced activation of Fpr2 leads to alleviation of fibrosis by stimulating immune resolution in systemic sclerosis.

Indexed as

AnimalsAnti-Inflammatory AgentsBleomycinCell DifferentiationCytokinesFibrosisMiceMice, Inbred C57BLMice, KnockoutMyofibroblastsOligopeptidesReceptors, Formyl PeptideScleroderma, SystemicSkinAnti-Inflammatory AgentsBleomycinCytokinesformyl peptide receptor 2, mouseOligopeptidesReceptors, Formyl PeptideTrp-Lys-Tyr-Met-Val-MetfibrosisFpr2sclerodermasystemic sclerosisWKYMVm

Identifiers

PMID31552041
PMCPMC6733889
OpenAlexW2969541374

What OpenQuestion 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 OpenQuestion graph.