Evidence map›Paper›PMID 39457482›Full record

ArticleBiomedicines2024

Increased Susceptibility to Mechanical Stretch Drives the Persistence of Keloid Fibroblasts: An Investigation Using a Stretchable PDMS Platform.

Jihee Kim, Chihyeong Won, Seoyoon Ham, Heetak Han, Sungsik Shin, Jieun Jang, Sanghyeon Lee, Chaebeen Kwon, Sungjoon Cho, Hyeonjoo Park and 4 more

Abstract read
In one paragraph

Article in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

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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

14 authors.

Jihee KimDepartment of Dermatology, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.ORCID 0000-0002-0047-5941
Chihyeong WonSchool of Electrical and Electronic Engineering, Yonsei University, Seoul 03722, Republic of Korea.ORCID 0000-0003-2141-7983
Seoyoon HamDepartment of Dermatology, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.ORCID 0009-0002-5569-9579
Heetak HanSchool of Electrical and Electronic Engineering, Yonsei University, Seoul 03722, Republic of Korea.
Sungsik ShinDepartment of Dermatology, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.
Jieun JangDepartment of Dermatology, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.
Sanghyeon LeeSchool of Electrical and Electronic Engineering, Yonsei University, Seoul 03722, Republic of Korea.
Chaebeen KwonSchool of Electrical and Electronic Engineering, Yonsei University, Seoul 03722, Republic of Korea.
Sungjoon ChoSchool of Electrical and Electronic Engineering, Yonsei University, Seoul 03722, Republic of Korea.
Hyeonjoo ParkSchool of Electrical and Electronic Engineering, Yonsei University, Seoul 03722, Republic of Korea.
Dongwon LeeDepartment of Plastic and Reconstructive Surgery, Institute for Human Tissue Restoration, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.ORCID 0000-0003-0046-3139
Won Jai LeeDepartment of Plastic and Reconstructive Surgery, Institute for Human Tissue Restoration, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.
Taeyoon LeeSchool of Electrical and Electronic Engineering, Yonsei University, Seoul 03722, Republic of Korea.ORCID 0000-0002-8269-0257
Ju Hee LeeDepartment of Dermatology, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.

Funding

National Research Foundation of Korea No. RS-2023-00234581, RS-2024-00336147 and RS-2024-00430782NAVER Digital Bio Innovation Research Fund No. 3720230070Severance Hospital Research fund for Clinical excellence(SHRC) C-2022-0038
6 · The paper itself

Abstract

backgroundKeloids are a common fibrotic disease of the skin, with the pathological hallmark of excessive extracellular matrix synthesis due to abnormal fibroblast activity. Since keloids clinically arise in areas of high mechanical tension, the mechanotransductory pathway may be attributed to its pathogenesis. We aimed to establish a preclinical platform to elucidate the underlying mechanism of keloid development and its clinical persistence.

methodsWe fabricated a mechanically stretchable polydimethylsiloxane cell culture platform; with its mimicry of the in vivo cyclic stretch of skeletal muscles, cells showed higher proliferation compared with conventional modalities.

resultsIn response to mechanical strain, TGF-β and type 1 collagen showed significant increases, suggesting possible TGF-β/Smad pathway activation via mechanical stimulation. Protein candidates selected by proteomic analysis were evaluated, indicating that key molecules involved in cell signaling and oxidative stress were significantly altered. Additionally, the cytoskeletal network of keloid fibroblasts showed increased expression of its components after periodic mechanical stimulation.

conclusionsHerein, we demonstrated and validated the existing body of knowledge regarding profibrotic mechanotransduction signaling pathways in keloid fibroblasts. Cyclic stretch, as a driving force, could help to decipher the tension-mediated biomechanical processes, leading to the development of optimized therapeutic targets.

Indexed as

fibroblastkeloidmechanosensitivitypolydimethylsiloxane

Identifiers

PMID39457482
PMCPMC11504861

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