Adipose Mesenchymal Stem Cells Promote Wound Healing by Modulating Expression of SERPINE1 in Dermal Fibroblasts and Keratinocytes.
Liang Y., Sun Q., Sun J., Xu M., Xu J., Yu Y.
Animal Study on Chronic Wound, published in Stem Cells Int (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
- Stem Cells Int (2026)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41509991
- PMCID
- PMC12775678
- DOI
- 10.1155/sci/5541440
Abstract (original English)
Background Adipose-derived mesenchymal stem cells (ADSCs) have great potential in the realm of tissue repair and regenerative medicine. However, the exact effects of ADSCs on the healing of skin wounds and the underlying mechanisms remain unexplored. Here, we investigated the effects of ADSCs on fibroblasts and keratinocytes and their related molecular mechanisms in wound healing. Methods We used a murine model in vivo and a Transwell coculture system in vitro. The proliferation and migration abilities of human dermal fibroblasts (HDFs) and human immortalized keratinocytes (HaCaT) were analyzed after coculture with ADSCs, and the target molecules were investigated by transcriptome sequencing. We further investigated phenotypic changes by knocking down and overexpressing the target molecule and analyzed the potential mechanisms. Results We successfully extracted, expanded, and identified ADSCs. ADSCs not only accelerated wound healing in mice but also improved healing quality. Coculture with ADSCs augmented the proliferation and migration capacities of main skin cells in vitro. RNA sequencing analysis revealed that the level of serpin family E member 1 (SERPINE1) in both HDF and HaCaT was significantly regulated by ADSCs. Knockdown of SERPINE1 restrained the proliferation and migration phenotypes of HDF and HaCaT, while overexpression of SERPINE1 did exactly the opposite. Pathwa
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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