Evidence map›Paper›PMID 34912333›Full record

ArticleFrontiers in immunology2021

PDGF Promotes Dermal Fibroblast Activation

Naoko Takamura, Ludivine Renaud, Willian Abraham da Silveira, Carol Feghali-Bostwick

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. 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
2.0field-weighted citation impact, top 13% 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, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Emerging Concepts in Therapeutic Interventions for Idiopathic Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025
    Review
  9. Roles of PDGF/PDGFR signaling in various organs.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Nuclear IL-33 in Fibroblasts Promotes Skin Fibrosis.The Journal of investigative dermatology · 2023
    Article
  14. Article
  15. Article
  16. The Molecular Mechanisms of Systemic Sclerosis-Associated Lung Fibrosis.International journal of molecular sciences · 2023
    Review
  17. Angiogenesis in Disease.International journal of molecular sciences · 2022
    Article
  18. Review
  19. PDGF/PDGFR: A Possible Molecular Target in Scleroderma Fibrosis.International journal of molecular sciences · 2022
    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 2 countries.

Naoko TakamuraDepartment of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Ludivine RenaudDepartment of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Willian Abraham da SilveiraDepartment of Biological Sciences, School of Life Sciences and Education, Staffordshire University, Stoke-on-Trent, United Kingdom.
Carol Feghali-BostwickDepartment of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Medical University of South Carolina · USUniversity of Staffordshire · GB

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI Sharon Gail Levy · 1990 to 2026
$71.5M
Training Grant in Inflammatory and Fibrosing DiseasesT32AR050958 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DIANE L KAMEN · 2005 to 2026
$4.2M
Scleroderma Twin Study and analysis of Estrogen in patients with dcSScK24AR060297 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FEGHALI-BOSTWICK, CAROL A. · 2013 to 2025
$1.4M
NCI NIH HHS P30 CA051008NIAMS NIH HHS K24 AR060297NIAMS NIH HHS T32 AR050958
6 · The paper itself

Abstract

Systemic sclerosis (SSc) is an autoimmune disease characterized by vasculopathy and excessive fibrosis of the skin and internal organs. To this day, no effective treatments to prevent the progression of fibrosis exist, and SSc patients have disabilities and reduced life expectancy. The need to better understand pathways that drive SSc and to find therapeutic targets is urgent. RNA sequencing data from SSc dermal fibroblasts suggested that melanin-concentrating hormone receptor 1 (MCHR1), one of the G protein-coupled receptors regulating emotion and energy metabolism, is abnormally deregulated in SSc. Platelet-derived growth factor (PDGF)-BB stimulation upregulated MCHR1 mRNA and protein levels in normal human dermal fibroblasts (NHDF), and MCHR1 silencing prevented the PDGF-BB-induced expression of the profibrotic factors transforming growth factor beta 1 (TGFβ1) and connective tissue growth factor (CTGF). PDGF-BB bound MCHR1 in membrane fractions of NHDF, and the binding was confirmed using surface plasmon resonance (SPR). MCHR1 inhibition blocked PDGF-BB modulation of intracellular cyclic adenosine monophosphate (cAMP). MCHR1 silencing in NHDF reduced PDGF-BB signaling. In summary, MCHR1 promoted the fibrotic response in NHDF through modulation of TGFβ1 and CTGF production, intracellular cAMP levels, and PDGF-BB-induced signaling pathways, suggesting that MCHR1 plays an important role in mediating the response to PDGF-BB and in the pathogenesis of SSc. Inhibition of MCHR1 should be considered as a novel therapeutic strategy in SSc-associated fibrosis.

Indexed as

FibroblastsHumansPlatelet-Derived Growth FactorReceptors, SomatostatinScleroderma, SystemicSignal TransductionSkinMCHR1 protein, humanPlatelet-Derived Growth FactorReceptors, SomatostatinfibroblastMCHR1PDGFsclerodermaskin fibrosissystemic sclerosis

Identifiers

PMID34912333
PMCPMC8667318
OpenAlexW3217582592

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.