Evidence map›Paper›PMID 40221432›Full record

ArticleNature communications2025

Fibromodulin selectively accelerates myofibroblast apoptosis in cutaneous wounds by enhancing interleukin 1β signaling.

Wenlu Jiang, Xiaoxiao Pang, Pin Ha, Chenshuang Li, Grace Xinlian Chang, Yuxin Zhang, Lawrence A Bossong, Kang Ting, Chia Soo, Zhong Zheng

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
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  7. Review
  8. Review
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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

10 authors.

Wenlu Jiang *Division of Plastic and Reconstructive Surgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Xiaoxiao Pang *Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing Municipal Key Laboratory of Oral, Biomedical Engineering of Higher Education, Stomatological Hospital of Chongqing Medical University, Chongqing, 401147, China.
Pin HaDivision of Plastic and Reconstructive Surgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.ORCID http://orcid.org/0000-0002-8934-0874
Chenshuang LiDepartment of Orthodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Grace Xinlian ChangDivision of Plastic and Reconstructive Surgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA.
Yuxin ZhangChongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing Municipal Key Laboratory of Oral, Biomedical Engineering of Higher Education, Stomatological Hospital of Chongqing Medical University, Chongqing, 401147, China.
Lawrence A BossongDepartment of Neuroscience, Princeton University, Princeton, NJ, 08540, USA.
Kang TingAmerican Dental Association Forsyth Institute, Cambridge, MA, 02142, USA. erickangting@gmail.com.ORCID http://orcid.org/0009-0003-5419-7152
Chia SooDivision of Plastic and Reconstructive Surgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA. bsoo@g.ucla.edu.ORCID http://orcid.org/0000-0003-2444-5963
Zhong ZhengDivision of Plastic and Reconstructive Surgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, 90095, USA. leozz95@gmail.com.ORCID http://orcid.org/0000-0002-4905-3563

Funding

Research Resource for Human Organs and Tissues (U42)U42OD011158 · OD · NATIONAL DISEASE RESEARCH INTERCHANGE · PI BELL, THOMAS J · 2012 to 2025
$25.0M
Anti-scar peptide for cleft lip repairSB1DE026972 · NIDCR · SCARLESS LABORATORIES, INC. · PI SOO, CHIA, TING, KANG · 2017 to 2019
$2.8M
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
Multiphoton Microscope for Deep Tissue ImagingS10OD025017 · OD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BENTOLILA, LAURENT A. · 2018 to 2018
$599k
NIAMS NIH HHS R44 AR064126NIDCR NIH HHS R44 DE024692NIDCR NIH HHS SB1 DE026972NIH HHS S10 OD025017NIH HHS U42 OD011158U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) R44AR064126U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR) R44DE024692U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR) SB1DE026972
6 · The paper itself

Abstract

Activated myofibroblasts deposit extracellular matrix material to facilitate rapid wound closure that can heal scarlessly during fetal development. However, adult myofibroblasts exhibit a relatively long life and persistent function, resulting in scarring. Thus, understanding how fetal and adult tissue regeneration differs may serve to identify factors that promote more optimal wound healing in adults with little or less scarring. We previously found that matricellular proteoglycan fibromodulin is one such factor promoting more optimal repair, but the underlying molecular and cellular mechanisms for these effects have not been fully elucidated. Here, we find that fibromodulin induces myofibroblast apoptosis after wound closure to reduce scarring in small and large animal models. Mechanistically, fibromodulin accelerates and prolongs the formation of the interleukin 1β-interleukin 1 receptor type 1-interleukin 1 receptor accessory protein ternary complex to increase the apoptosis of myofibroblasts and keloid- and hypertrophic scar-derived cells. As the persistence of myofibroblasts during tissue regeneration is a key cause of fibrosis in most organs, fibromodulin represents a promising, broad-spectrum anti-fibrotic therapeutic.

Indexed as

ApoptosisFibromodulinInterleukin-1betaMyofibroblastsSkinWound HealingAnimalsCicatrixCicatrix, HypertrophicDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLSignal TransductionFibromodulinInterleukin-1beta

Identifiers

PMID40221432
PMCPMC11993684

What OpenQuestion holds

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LicenceCC BY
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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.