Mitochondrial transfer from adipose-derived stem cells reprograms macrophage lipid metabolism to improve fat graft survival.
Guo T., Li J., Lin J., Xie M., Du Y., Fu J.
Animal Study, published in J Transl Med (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
- Animal Study
- Journal
- J Transl Med (2026)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42135740
- DOI
- 10.1186/s12967-026-08224-9
Abstract (original English)
Background Autologous fat grafting is common for soft tissue repair, but often results in adipocyte necrosis due to ischaemia and hypoxia, causing inflammation and poor graft retention. Our research indicates that adipose-derived mesenchymal stem cells (ASCs) induce mitochondrial fatty acid β-oxidation (FAO) in macrophages, thus facilitating their M2 polarization and ultimately enhancing graft survival. ASCs also transfer mitochondria to recipient cells by tunnelling nanotubes (TNTs), increasing energy metabolism and the oxidative stress response. On the basis of these findings, we propose that ASCs facilitate mitochondrial transfer to macrophages through TNTs, which in turn enhances FAO, thus promoting M2 polarization and ultimately improving fat graft retention. Methods This study established a model of ASCs-assisted fat grafting in mice and an in vitro coculture system comprising ASCs and high-fat-treated macrophages. ASCs were treated with the actin polymerization inhibitor latrunculin A (latA) to block TNTs formation. We evaluated lipid deposition, mitochondrial transfer in macrophages, and mitochondrial function using electron microscopy, immunofluorescence, and qPCR. Results The findings indicated that ASCs enhance FAO in macrophages and improve fat graft retention, but latA pretreatment inhibited mitochondrial transfer, decreasing these effects. Conclusion This research
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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