Adipose Stem Cell-Derived Apoptotic Vesicles Attenuate Hypertrophic Scarring by Targeting the CDC20/WNT Signaling Pathway.
Jiang M., Cheng L., Mao X., Zhang L.
Laboratory Study on Scar, published in Biomedicines (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Biomedicines (2026)
- Country
- Switzerland
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42193410
- PMCID
- PMC13204812
- DOI
- 10.3390/biomedicines14051083
Abstract (original English)
Background : Apoptotic vesicles (ApoVs) derived from adipose stem cells (ASCs) have recently emerged as important mediators of tissue repair and are implicated in pathways relevant to hypertrophic scar (HS). Although ASCs exhibit potential in scar modulation, the therapeutic value of their apoptotic clearance products remains largely unexplored. Methods : In this study, we investigated the efficacy and mechanism of staurosporine (STS)-induced adipose stem cell derived apoptotic vesicles (ASCs-ApoVs) in mitigating HS. Western blot, RT-qPCR, and immunofluorescence were used to assess fibrotic markers including α-SMA, COL1A1, and COL3A1 and so on in hypertrophic scar derived fibroblasts (HS-fibroblasts). Results : ASCs-ApoVs significantly reduced profibrotic marker expression in HS-fibroblasts without short-term cytotoxicity. CDC20 down-regulation was identified as a critical target, through which ASCs-ApoVs suppressed Wnt/β-catenin signaling, as evidenced by the downregulation of β-catenin, c-MYC, Cyclin D1, and AXIN2. The efficacy of ASCs-ApoVs in hypertrophic scar regulation was also confirmed by the rabbit ear scar model. Furthermore, ASCs-ApoVs demonstrated notable structural and functional stability. Conclusions : In summary, our results established STS-induced ASCs-ApoVs as a potent multi-target strategy for hypertrophic scar regulation. Besides, the scalable production, fu
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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