Evidence map›Paper›PMID 40742741›Full record

ArticleThe Journal of pathology2025

Increased expression of the PIEZO2 mechanoreceptor in fibroblasts and endothelial cells within the lymphatic and vascular vessels of keloids.

Shinsuke Akita, Sanae Ikehara, Masahiro Kiuchi, Kota Kokubo, Kazuhiko Azuma, Syouta Ohki, Hiroyuki Matsuyama, Joceline Theda Kadarman, Yohei Hosokawa, Yoshihiro Akimoto and 6 more

Abstract read
In one paragraph

Article in The Journal of pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–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

7 citing papers in PubMed.

  1. Review
  2. Yoda molecules agonize PIEZO2.bioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. PIEZO2 in tumors: from mechanobiological switches to activity-targeted therapies.Journal of experimental & clinical cancer research : CR · 2025
    Review
  7. 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.

Shinsuke Akita *Department of Plastic, Reconstructive, and Aesthetic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0001-7075-6602
Sanae Ikehara *Department of Pathology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0001-7123-4777
Masahiro KiuchiDepartment of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-0227-4502
Kota KokuboDepartment of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0001-6896-1981
Kazuhiko AzumaDepartment of Pathology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0009-0001-3362-6662
Syouta OhkiDepartment of Pathology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0009-0007-0800-7361
Hiroyuki MatsuyamaDepartment of Pathology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Joceline Theda KadarmanDepartment of Plastic, Reconstructive, and Aesthetic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0009-0007-1556-2590
Yohei HosokawaDepartment of Pathology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0009-0004-1543-3818
Yoshihiro AkimotoDepartment of Microscopic Anatomy, Kyorin University School of Medicine, Tokyo, Japan.ORCID 0000-0002-0281-4150
Yosuke InabaClinical Research Center, Chiba University Hospital, Chiba, Japan.ORCID 0000-0002-8659-2873
Hideki HanaokaClinical Research Center, Chiba University Hospital, Chiba, Japan.ORCID 0000-0003-0186-9296
Nobuyuki MitsukawaDepartment of Plastic, Reconstructive, and Aesthetic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-0234-8241
Kiyoshi HiraharaDepartment of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-9128-9449
Toshinori NakayamaDepartment of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-1434-2007
Yuzuru IkeharaDepartment of Pathology, Graduate School of Medicine, Chiba University, Chiba, Japan.ORCID 0000-0002-1915-9172

Funding

Japan Agency for Medical Research and Development JP19hm0102069h001Japan Agency for Medical Research and Development JP21gm1210003Japan Science Society JPMJMS2025Ministry of Education, Culture, Sports, Science and Technology 19K07682Ministry of Education, Culture, Sports, Science and Technology 20K08351Ministry of Education, Culture, Sports, Science and Technology 23K07455Ministry of Education, Culture, Sports, Science and Technology JP19H05650
6 · The paper itself

Abstract

Keloids are scars that grow abnormally due to excessive extracellular matrix production by fibroblasts and increased angiogenesis. Chronic tension is implicated in their growth, but the exact pathology remains unclear. This study investigated the increased expression of molecules responsible for sensing pressure in keloids compared with lymphedema, which is also a non-tumorous fibroproliferative disease caused by another etiology. Higher expression levels of COL1A2, PIEZO2, and POSTN were observed in the keloid group compared with the lymphedema group. PIEZO2 expression levels showed a strong correlation with both COL1A2 (r = 0.9252, 95% CI 0.8474-0.9641, p < 0.001) and POSTN (r = 0.9118, 95% CI 0.8213-0.9575, p < 0.001). Additionally, PIEZO2 expression levels were significantly higher in recurrent keloids than in non-recurrent keloids (3,032.5 ± 1,090.2 versus 1,241.9 ± 860.7, p = 0.032). Analysis of gene expression at the single-cell level found upregulation of PIEZO2 in vascular and lymphatic endothelial cells, and a subgroup of fibroblasts. Additionally, COL1A1, COL1A2, COL3A1, and POSTN expression was also increased in the fibroblast subgroup. Furthermore, in fibroblasts with high PIEZO2 expression, extracellular matrix collagen production signaling was augmented. Histological analysis confirmed the presence of PIEZO2-positive cells in the perivascular stroma active area of keloid tissue, together with inflammatory cells. Therefore, since PIEZO2-positive cells are highly expressed specifically in keloids and are deeply involved in their recurrence and activity, we propose that the pathogenesis of keloids is constructed by PIEZO2-positive cells. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

Indexed as

Endothelial CellsFibroblastsIon ChannelsKeloidLymphatic VesselsAdolescentAdultCollagen Type IExtracellular Matrix ProteinsFemaleHumansLymphedemaMaleMechanotransduction, CellularMiddle AgedYoung AdultCollagen Type IExtracellular Matrix ProteinsIon ChannelsPIEZO2 protein, humanendothelial cells in lymphatic and vascular vesselsfibroblastskeloidsmechanoreceptorPIEZO2

Identifiers

PMID40742741
PMCPMC12337814

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.