Evidence map›Paper›PMID 36694861›Full record

ArticleBurns & trauma2023

Skin 11β-hydroxysteroid dehydrogenase type 1 enzyme expression regulates burn wound healing and can be targeted to modify scar characteristics.

Kevin H-Y Tsai, Huaikai Shi, Roxanne J Parungao, Sina Naficy, Xiaotong Ding, Xiaofeng Ding, Jonathan J Hew, Xiaosuo Wang, Wojciech Chrzanowski, Gareth G Lavery and 7 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Burns & trauma, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Marine-Derived Polyketides fromACS pharmacology & translational science · 2026
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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 4 institutions in 3 countries.

Kevin H-Y TsaiAdrenal Steroid Group, ANZAC Research Institute, Concord Hospital, The University of Sydney, Sydney, NSW 2137, Australia.
Huaikai ShiBurns and Reconstructive Surgery Research Group, ANZAC Research Institute, Concord Hospital, The University of Sydney, Sydney, NSW 2137, Australia.ORCID https://orcid.org/0000-0002-8269-2981
Roxanne J ParungaoBurns and Reconstructive Surgery Research Group, ANZAC Research Institute, Concord Hospital, The University of Sydney, Sydney, NSW 2137, Australia.
Sina NaficySchool of Chemical and Biomolecular Engineering, The University of Sydney, Sydney, NSW 2006, Australia.
Xiaotong DingJiangsu Provincial Engineering Research Centre of TCM External Medication Development and Application, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210023, China.
Xiaofeng DingDepartment of Burns and Plastic Surgery, Nanjing Drum Tower Hospital Clinical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210008, China.
Jonathan J HewBurns and Reconstructive Surgery Research Group, ANZAC Research Institute, Concord Hospital, The University of Sydney, Sydney, NSW 2137, Australia.
Xiaosuo WangHeart Research Institute, The University of Sydney, Sydney, NSW 2006 , Australia.
Wojciech ChrzanowskiSydney Nano Institute, Sydney Pharmacy School, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW 2006, Australia.
Gareth G LaveryDepartment of Biosciences, Centre for Healthy Ageing and Understanding Disease, Nottingham Trent University, NG1 4BU, UK.
Zhe LiBurns and Reconstructive Surgery Unit, Concord Repatriation General Hospital, Sydney, NSW 2137, Australia.
Andrea C Issler-FisherBurns and Reconstructive Surgery Unit, Concord Repatriation General Hospital, Sydney, NSW 2137, Australia.
Jun ChenJiangsu Provincial Engineering Research Centre of TCM External Medication Development and Application, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210023, China.
Qian TanDepartment of Burns and Plastic Surgery, Nanjing Drum Tower Hospital Clinical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210008, China.
Peter K MaitzBurns and Reconstructive Surgery Research Group, ANZAC Research Institute, Concord Hospital, The University of Sydney, Sydney, NSW 2137, Australia.
Mark S CooperAdrenal Steroid Group, ANZAC Research Institute, Concord Hospital, The University of Sydney, Sydney, NSW 2137, Australia.
Yiwei WangBurns and Reconstructive Surgery Research Group, ANZAC Research Institute, Concord Hospital, The University of Sydney, Sydney, NSW 2137, Australia.ORCID https://orcid.org/0000-0001-6585-6641
The University of Sydney · AUNanjing University of Chinese Medicine · CNConcord Repatriation General Hospital · AUNottingham Trent University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Excessive scarring and fibrosis are the most severe and common complications of burn injury. Prolonged exposure to high levels of glucocorticoids detrimentally impacts on skin, leading to skin thinning and impaired wound healing. Skin can generate active glucocorticoids locally through expression and activity of the 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1). We hypothesised that burn injury would induce 11β-HSD1 expression and local glucocorticoid metabolism, which would have important impacts on wound healing, fibrosis and scarring. We additionally proposed that pharmacological manipulation of this system could improve aspects of post-burn scarring. Methods: Skin 11β-HSD1 expression in burns patients and mice was examined. The impacts of 11β-HSD1 mediating glucocorticoid metabolism on burn wound healing, scar formation and scar elasticity and quality were additionally examined using a murine 11β-HSD1 genetic knockout model. Slow-release scaffolds containing therapeutic agents, including active and inactive glucocorticoids, were developed and pre-clinically tested in mice with burn injury. Results: We demonstrate that 11β-HSD1 expression levels increased substantially in both human and mouse skin after burn injury. 11β-HSD1 knockout mice experienced faster wound healing than wild type mice but the healed wounds manifested significantly more collagen deposition, tensile strength and stiffness, features characteristic of excessive scarring. Application of slow-release prednisone, an inactive glucocorticoid, slowed the initial rate of wound closure but significantly reduced post-burn scarring via reductions in inflammation, myofibroblast generation, collagen production and scar stiffness. Conclusions: Skin 11β-HSD1 expression is a key regulator of wound healing and scarring after burn injury. Application of an inactive glucocorticoid capable of activation by local 11β-HSD1 in skin slows the initial rate of wound closure but significantlyimproves scar characteristics post burn injury.

Indexed as

11β-HSD1 knockoutBurn injuryDrug deliveryGlucocorticoid metabolismPolycaprolactone scaffoldScarringSkin 11β-HSD1Wound healing

Identifiers

PMID36694861
PMCPMC9862341
OpenAlexW4317659237

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.