Evidence map›Paper›PMID 36609486›Full record

ArticleCommunications biology2023

Highly concentrated trehalose induces prohealing senescence-like state in fibroblasts via CDKN1A/p21.

Jun Muto, Shinji Fukuda, Kenji Watanabe, Xiuju Dai, Teruko Tsuda, Takeshi Kiyoi, Kenji Kameda, Ryosuke Kawakami, Hideki Mori, Ken Shiraishi and 6 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

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  14. Cellular Senescence in Skin Wound Repair: Dual Roles and Senotherapeutic Interventions.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
    Review
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

16 authors at 6 institutions in 1 country.

Jun MutoDepartment of Dermatology, Ehime University Graduate School of Medicine, Toon, Japan. muto.jun.xs@ehime-u.ac.jp.ORCID 0000-0001-9565-9796
Shinji FukudaDepartment of Biochemistry, School of Dentistry, Aichi Gakuin University, Nagoya, Japan.ORCID 0000-0002-6920-1818
Kenji WatanabeInstitute of Gene Research, Yamaguchi University Science Research Center, Yamaguchi, Japan.
Xiuju DaiDepartment of Dermatology, Ehime University Graduate School of Medicine, Toon, Japan.
Teruko TsudaDepartment of Dermatology, Ehime University Graduate School of Medicine, Toon, Japan.
Takeshi KiyoiDepartment of Pharmacology, School of Medicine, Kanazawa Medical University, Uchinada, Japan.
Kenji KamedaDepartment of Dermatology, Ehime University Graduate School of Medicine, Toon, Japan.
Ryosuke KawakamiDepartment of Molecular Medicine for Pathogenesis, Ehime University Graduate School of Medicine, Toon, Japan.
Hideki MoriDepartment of Dermatology, Ehime University Graduate School of Medicine, Toon, Japan.
Ken ShiraishiDepartment of Dermatology, Ehime University Graduate School of Medicine, Toon, Japan.
Masamoto MurakamiDepartment of Dermatology, Ehime University Graduate School of Medicine, Toon, Japan.ORCID 0000-0003-3923-5096
Takeshi ImamuraDepartment of Molecular Medicine for Pathogenesis, Ehime University Graduate School of Medicine, Toon, Japan.
Shigeki HigashiyamaDivision of Cell Growth and Tumor Regulation, Proteo-Science Center, Ehime University, Toon, Japan.
Yasuhiro FujisawaDepartment of Dermatology, Ehime University Graduate School of Medicine, Toon, Japan.
Yoichi MizukamiInstitute of Gene Research, Yamaguchi University Science Research Center, Yamaguchi, Japan.
Koji SayamaDepartment of Dermatology, Ehime University Graduate School of Medicine, Toon, Japan.ORCID 0000-0001-9915-8964
Ehime University · JPYamaguchi University · JPAichi Gakuin University · JPEhime University Hospital · JPKanazawa Medical University · JPOsaka International Cancer Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trehalose is the nonreducing disaccharide of glucose, evolutionarily conserved in invertebrates. The living skin equivalent (LSE) is an organotypic coculture containing keratinocytes cultivated on fibroblast-populated dermal substitutes. We demonstrated that human primary fibroblasts treated with highly concentrated trehalose promote significantly extensive spread of the epidermal layer of LSE without any deleterious effects. The RNA-seq analysis of trehalose-treated 2D and 3D fibroblasts at early time points revealed the involvement of the CDKN1A pathway, the knockdown of which significantly suppressed the upregulation of DPT, ANGPT2, VEGFA, EREG, and FGF2. The trehalose-treated fibroblasts were positive for senescence-associated β-galactosidase. Finally, transplantation of the dermal substitute with trehalose-treated fibroblasts accelerated wound closure and increased capillary formation significantly in the experimental mouse wounds in vivo, which was canceled by the CDKN1A knockdown. These data indicate that high-concentration trehalose can induce the senescence-like state in fibroblasts via CDKN1A/p21, which may be therapeutically useful for optimal wound repair.

Indexed as

SkinTrehaloseAnimalsCyclin-Dependent Kinase Inhibitor p21FibroblastsHumansKeratinocytesMiceWound HealingCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Trehalose

Identifiers

PMID36609486
PMCPMC9822918
OpenAlexW4313646589

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.