SVF
Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Adipose-derived stem cells (ADSCs)-derived DKK1 promotes cutaneous wound healing by inducing M2 macrophage polarization via PI3K/AKT and JNK activation.

Liu D., Liu N., Liu X., Liu Y., Zhang H., Zhou Z.

Animal Study on Chronic Wound, Immune Modulation, published in Biochim Biophys Acta Mol Cell Res (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

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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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
Animal Study
Journal
Biochim Biophys Acta Mol Cell Res (2025)
Country
Netherlands
Reported sample size
—
Source database
PubMed
PMID
41177176
DOI
10.1016/j.bbamcr.2025.120077

Abstract (original English)

Wound healing requires the coordinated resolution of inflammation and tissue regeneration, whereby the role played by macrophage polarization is critical. This study investigates whether adipose-derived stem cells (ADSCs) promote wound repair through paracrine dickkopf-related protein 1 (DKK1) and explores their regulatory mechanism on macrophage polarization. In a murine full-thickness skin wound model, ADSCs treatment significantly enhanced re-epithelialization, collagen deposition, and Ki67 expression levels, while reducing local inflammatory cytokines and promoting M2 macrophage polarization. In vitro, ADSCs suppressed proinflammatory cytokines and induced M2 markers in LPS/IFN-γ-stimulated macrophages, an effect that was attenuated upon DKK1 knockdown. Mechanistically, DKK1 enhanced PI3K/AKT and JNK pathway activation both in macrophages and wound tissue. DKK1-deficient ADSCs showed a diminished ability to promote wound healing, reduce inflammation, and modulate macrophage phenotypes. These findings identify DKK1 as a key paracrine mediator of ADSCs-driven immunomodulation and tissue regeneration, thereby providing new insights into optimizing stem cell-based therapies for wound healing.

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.

How we grade evidence
AnimalsMiceProto-Oncogene Proteins c-aktWound HealingIntercellular Signaling Peptides and ProteinsPhosphatidylinositol 3-KinasesMacrophagesAdipose TissueStem CellsSkin
Chronic WoundImmune Modulation
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