Evidence map›Paper›PMID 29201497›Full record

ArticleSignal transduction and targeted therapy

Fibromodulin reduces scar formation in adult cutaneous wounds by eliciting a fetal-like phenotype.

Zhong Zheng, Aaron W James, Chenshuang Li, Wenlu Jiang, Joyce Z Wang, Grace X Chang, Kevin S Lee, Feng Chen, Emily A Berthiaume, Yao Chen and 7 more

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

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  17. An Update on Molecular Mechanisms of Scarring-A Narrative Review.International journal of molecular sciences · 2024
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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

17 authors at 6 institutions in 2 countries.

Zhong ZhengDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Aaron W JamesDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Chenshuang LiDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Wenlu JiangDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Joyce Z WangDepartment of Emergency Medicine, Highland General Hospital, Oakland, CA 94602, USA.
Grace X ChangDavid Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Kevin S LeeDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Feng ChenDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Emily A BerthiaumeDavid Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Yao ChenDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Hsin Chuan PanDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Eric C ChenDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Weiming LiDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Zhihe ZhaoState Key Laboratory of Oral Diseases, Department of Orthodontics, West China School of Stomatology, Sichuan University, Chengdu, Sichuan 610041, P. R. China.
Xinli ZhangDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Kang TingDivision of Growth and Development, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Chia SooUCLA Division of Plastic and Reconstructive Surgery and Department of Orthopaedic Surgery and the Orthopaedic Hospital Research Center, University of California, Los Angeles, Los Angeles, CA 90095, USA.
University of California, Los Angeles · USHarbin Medical University · CNHighland Hospital · USJohns Hopkins University · USKing University · USSichuan University · CN

Funding

UCLA FUNDAMENTAL CLINICAL RESEARCH TRAINING PROGRAMT32DE007296 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WONG, DAVID T · 1996 to 2011
$5.8M
Novel peptide-impregnated hydrogel as a wound healing deviceR44DE026080 · NIDCR · SCARLESS LABORATORIES, INC. · PI SOO, CHIA, ZHENG, ZHONG · 2016 to 2023
$4.7M
Anti-scar peptide for cleft lip repairR44DE024692 · NIDCR · SCARLESS LABORATORIES, INC. · PI SOO, CHIA, ZHENG, ZHONG · 2014 to 2016
$1.5M
A novel anti-scar peptide for cutaneous wound repairR44AR064126 · NIAMS · SCARLESS LABORATORIES, INC. · PI SOO, CHIA, ZHENG, ZHONG · 2015 to 2016
$1.5M
A novel anti-scar peptide for cutaneous wound repairR43AR064126 · NIAMS · SCARLESS LABORATORIES, INC. · PI PANG, SHEN, SOO, CHIA · 2013 to 2014
$398k
Safety and efficacy testing of novel anti-scar peptide vs corticosteroid for scarR43AR063558 · NIAMS · SCARLESS LABORATORIES, INC. · PI PANG, SHEN, SOO, CHIA · 2014 to 2015
$397k
NIAMS NIH HHS R43 AR063558NIAMS NIH HHS R43 AR064126NIAMS NIH HHS R44 AR064126NIDCR NIH HHS R44 DE024692NIDCR NIH HHS R44 DE026080NIDCR NIH HHS T32 DE007296
6 · The paper itself

Abstract

Blocking transforming growth factor (TGF)β1 signal transduction has been a central strategy for scar reduction; however, this approach appears to be minimally effective. Here, we show that fibromodulin (FMOD), a 59-kD small leucine-rich proteoglycan critical for normal collagen fibrillogenesis, significantly reduces scar formation while simultaneously increasing scar strength in both adult rodent models and porcine wounds, which simulate human cutaneous scar repair. Mechanistically, FMOD uncouples pro-migration/contraction cellular signals from pro-fibrotic signaling by selectively enhancing SMAD3-mediated signal transduction, while reducing AP-1-mediated TGFβ1 auto-induction and fibrotic extracellular matrix accumulation. Consequently, FMOD accelerates TGFβ1-responsive adult fibroblast migration, myofibroblast conversion, and function. Furthermore, our findings strongly indicate that, by delicately orchestrating TGFβ1 activities rather than indiscriminately blocking TGFβ1, FMOD elicits fetal-like cellular and molecular phenotypes in adult dermal fibroblasts

Indexed as

Fetal-like phenotypeFibromodulinScar reductionTransforming growth factor β1Wound healing

Identifiers

PMID29201497
PMCPMC5661627
OpenAlexW2761068618

What OpenQuestion holds

Textmetadata
LicenceTDM
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.