Evidence map›Paper›PMID 26697429›Full record

ArticleFrontiers in medicine2015

Mechanical Stress Changes the Complex Interplay Between HO-1, Inflammation and Fibrosis, During Excisional Wound Repair.

Niels A J Cremers, Maarten Suttorp, Marlous M Gerritsen, Ronald J Wong, Coby van Run-van Breda, Gooitzen M van Dam, Katrien M Brouwer, Anne Marie Kuijpers-Jagtman, Carine E L Carels, Ditte M S Lundvig and 1 more

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In one paragraph

Article in Frontiers in medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
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  4. CD44 signaling in skin wound healing and regeneration.Journal of translational medicine · 2025
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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

11 authors at 5 institutions in 2 countries.

Niels A J CremersDepartment of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences , Nijmegen , Netherlands ; Experimental Rheumatology, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences , Nijmegen , Netherlands.
Maarten SuttorpDepartment of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences , Nijmegen , Netherlands.
Marlous M GerritsenDepartment of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences , Nijmegen , Netherlands.
Ronald J WongDepartment of Pediatrics, Stanford University School of Medicine , Stanford, CA , USA.
Coby van Run-van BredaDepartment of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences , Nijmegen , Netherlands.
Gooitzen M van DamDepartment of Surgery, University Medical Center Groningen , Groningen , Netherlands.
Katrien M BrouwerDepartment of Plastic, Reconstructive and Hand Surgery, VU University Medical Center, MOVE Research Institute Amsterdam , Amsterdam , Netherlands ; Association of Dutch Burn Centers , Beverwijk , Netherlands.
Anne Marie Kuijpers-JagtmanDepartment of Orthodontics and Craniofacial Biology, Cleft Palate Craniofacial Center, Radboud University Medical Center , Nijmegen , Netherlands.
Carine E L CarelsDepartment of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences , Nijmegen , Netherlands.
Ditte M S LundvigDepartment of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences , Nijmegen , Netherlands.
Frank A D T G WagenerDepartment of Orthodontics and Craniofacial Biology, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences , Nijmegen , Netherlands.
Radboud Institute for Molecular Life Sciences · NLRadboud University Nijmegen · NLAssociation of Dutch Burn Centres · NLStanford University · USUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanical stress following surgery or injury can promote pathological wound healing and fibrosis, and lead to functional loss and esthetic problems. Splinted excisional wounds can be used as a model for inducing mechanical stress. The cytoprotective enzyme heme oxygenase-1 (HO-1) is thought to orchestrate the defense against inflammatory and oxidative insults that drive fibrosis. Here, we investigated the activation of the HO-1 system in a splinted and non-splinted full-thickness excisional wound model using HO-1-luc transgenic mice. Effects of splinting on wound closure, HO-1 promoter activity, and markers of inflammation and fibrosis were assessed. After seven days, splinted wounds were more than three times larger than non-splinted wounds, demonstrating a delay in wound closure. HO-1 promoter activity rapidly decreased following removal of the (epi)dermis, but was induced in both splinted and non-splinted wounds during skin repair. Splinting induced more HO-1 gene expression in 7-day wounds; however, HO-1 protein expression remained lower in the epidermis, likely due to lower numbers of keratinocytes in the re-epithelialization tissue. Higher numbers of F4/80-positive macrophages, αSMA-positive myofibroblasts, and increased levels of the inflammatory genes IL-1β, TNF-α, and COX-2 were present in 7-day splinted wounds. Surprisingly, mRNA expression of newly formed collagen (type III) was lower in 7-day wounds after splinting, whereas, VEGF and MMP-9 were increased. In summary, these data demonstrate that splinting delays cutaneous wound closure and HO-1 protein induction. The pro-inflammatory environment following splinting may facilitate higher myofibroblast numbers and increase the risk of fibrosis and scar formation. Therefore, inducing HO-1 activity against mechanical stress-induced inflammation and fibrosis may be an interesting strategy to prevent negative effects of surgery on growth and function in patients with orofacial clefts or in patients with burns.

Indexed as

burnscleft palatefibrosisheme oxygenase-1inflammationmechanical stresswound healing

Identifiers

PMID26697429
PMCPMC4678194
OpenAlexW2237857564

What OpenQuestion holds

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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.