Evidence map›Paper›PMID 28610597›Full record

ArticleArthritis research & therapy2017

Anti-connective tissue growth factor (CTGF/CCN2) monoclonal antibody attenuates skin fibrosis in mice models of systemic sclerosis.

Katsunari Makino, Tomoko Makino, Lukasz Stawski, Kenneth E Lipson, Andrew Leask, Maria Trojanowska

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
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  14. Towards a Unified Approach in Autoimmune Fibrotic Signalling Pathways.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. The Dawning of a New Enterprise: RNA Therapeutics for the Skin.Journal of dermatology and skin science · 2023
    Article
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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.

Katsunari MakinoArthritis Center, Boston University School of Medicine, 72 East Concord Street, E-5, Boston, MA, 02118, USA.
Tomoko MakinoArthritis Center, Boston University School of Medicine, 72 East Concord Street, E-5, Boston, MA, 02118, USA.
Lukasz StawskiArthritis Center, Boston University School of Medicine, 72 East Concord Street, E-5, Boston, MA, 02118, USA.
Kenneth E LipsonFibroGen, Inc, San Francisco, CA, USA.
Andrew LeaskDepartments of Dentistry and Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, Dental Sciences Building, London, ON, Canada.
Maria TrojanowskaArthritis Center, Boston University School of Medicine, 72 East Concord Street, E-5, Boston, MA, 02118, USA. trojanme@bu.edu.ORCID 0000-0001-9550-7178
Boston University · USFibroGen (United States) · USWestern University · CA

Funding

The molecular mechanisms of fibrosisR01AR042334 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1994 to 2018
$5.2M
TGF BETA RECEPTOR SIGNALING IN SCLERODERMAR01AR044883 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1998 to 2012
$3.3M
TGF-beta receptor/Endoglin signaling and the origin of scleroderma fibroblastR56AR044883 · NIAMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI TROJANOWSKA, MARIA · 2015 to 2015
$410k
NIAMS NIH HHS R01 AR042334NIAMS NIH HHS R01 AR044883NIAMS NIH HHS R56 AR044883
6 · The paper itself

Abstract

backgroundSystemic sclerosis (SSc) is characterized by fibrosis of the skin and internal organs. Although the involvement of connective tissue growth factor (CTGF/CCN2) has been well-documented in SSc fibrosis, the therapeutic potential of targeting CTGF in SSc has not been fully investigated. Our aim was to examine the therapeutic potential of CTGF blockade in a preclinical model of SSc using two approaches: smooth muscle cell fibroblast-specific deletion of CTGF (CTGF knockout (KO)) or a human anti-CTGF monoclonal antibody, FG-3019.

methodsAngiotensin II (Ang II) was administered for 14 days by subcutaneous osmotic pump to CTGF KO or C57BL/6 J mice. FG-3019 was administered intraperitoneally three times per week for 2 weeks. Skin fibrosis was evaluated by histology and hydroxyproline assay. Immunohistochemistry staining was used for alpha smooth muscle actin (αSMA), platelet-derived growth factor receptor β (PDGFRβ), pSmad2, CD45, von Willebrand factor (vWF), and immunofluorescence staining was utilized for procollagen and Fsp1.

resultsAng II-induced skin fibrosis was mitigated in both CTGF KO and FG-3019-treated mice. The blockade of CTGF reduced the number of cells expressing PDGFRβ, procollagen, αSMA, pSmad2, CD45, and Fsp1 in the dermis. In addition, inhibition of CTGF attenuated vascular injury as measured by the presence of vWF-positive cells.

conclusionsOur data indicate that inhibition of CTGF signaling presents an attractive therapeutic approach in SSc.

Indexed as

ActinsAngiotensin IIAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedCells, CulturedConnective Tissue Growth FactorDisease Models, AnimalFibroblastsFibrosisHumansMice, Inbred C57BLMice, KnockoutMice, TransgenicScleroderma, SystemicSkinActa2 protein, mouseActinsAngiotensin IIAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedConnective Tissue Growth FactorpamrevlumabAngiotensin IICTGF/CCN2FG-3019FibrosisSkinSystemic sclerosis

Identifiers

PMID28610597
PMCPMC5470189
OpenAlexW2626842638

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.