[Cytochalasin B-Induced adipose stem cell-derived nanovesicles promote hair follicle regeneration via activation of the β-catenin signaling pathway].
Wang L., Liu Y., Cai P., Mao X., Tian T., Cao L.
Animal Study on Chronic Wound, published in Zhejiang Da Xue Xue Bao Yi Xue Ban (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
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- Study type
- Animal Study
- Journal
- Zhejiang Da Xue Xue Bao Yi Xue Ban (2026)
- Country
- China
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42409593
- DOI
- 10.3724/zdxbyxb-2025-0780
Abstract (original English)
To evaluate the regulatory effects of adipose stem cell (ADSC)-derived cytochalasin B-induced nanovesicles (CINVs) on the biological functions of dermal papilla cells (DPCs) and on hair follicle cycle transition, and to explore the underlying molecular mechanisms. CINVs were prepared from ADSCs. Their effects on DPC proliferation, migration, and apoptosis were assessed in vitro . A mouse depilation model was used to evaluate the ability of CINVs to promote the transition of hair follicles from telogen to anagen. Western blotting, hematoxylin-eosin (HE) staining, and immunofluo-rescence analyses were performed to assess the activation of β-catenin-related signaling pathways and to elucidate the molecular mechanisms of CINV-mediated hair follicle regeneration. CCK-8 assays showed that CINVs at 40 and 60 μg/mL significantly enhanced DPC proliferation. Wound healing assays (at 40 μg/mL) confirmed that CINVs markedly promoted DPC migration. Western blotting revealed that, compared with the control group, CINV treatment significantly increased the expression of phosphorylated GSK-3β (p-GSK-3β, P <0.05) and upregulated β-catenin, the core effector of the canonical Wnt/β-catenin pathway ( P <0.01). Moreover, cyclin D1 (a positive regulator of cell cycle progression) expression was elevated ( P <0.05), and the levels of phosphorylated AKT (p-AKT, associated with cell survival) and phosp
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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