Low-intensity pulsed ultrasound regulates the osteogenic-adipogenic differentiation balance of rat adipose-derived stem cells via the PI3K/AKT-SREBF1 signaling axis.
Hu W., Zhao Z., Zhang Q., Gong P., Wang X., Han C.
Animal Study, published in Stem Cells 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
- Stem Cells Transl Med (2026)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42367072
- DOI
- 10.1093/stcltm/szag032
Abstract (original English)
Rat adipose-derived stem cells (rADSCs) are widely used in bone tissue engineering (BTE). Low-intensity pulsed ultrasound (LIPUS) can modulate stem cell fate; however, its precise regulatory effects on ADSC lineage commitment remain unclear. This study aimed to elucidate how LIPUS regulates the osteogenic-adipogenic differentiation balance of rADSCs. We first performed cell proliferation and differentiation induction assays, which demonstrated that LIPUS significantly enhanced osteogenic differentiation while simultaneously suppressing adipogenesis, without affecting rADSC proliferation. Subsequently, transcriptome sequencing and protein-protein interaction analysis identified sterol regulatory element binding transcription factor 1 (Srebf1) as a pivotal regulatory node in LIPUS-modulated osteogenic-adipogenic differentiation. Rescue experiments further confirmed that LIPUS rescued the Srebf1 overexpression phenotype by restoring osteogenic potential and attenuating adipogenesis. Mechanistically, LIPUS downregulated SREBF1 expression and inhibited its nuclear translocation by inhibiting PI3K/AKT signaling, as evidenced by synergistic effects with the PI3K-specific inhibitor LY294002. Finally, a rat cranial defect model was established to validate the osteogenic potential of LIPUS in vivo. LIPUS significantly enhanced bone defect repair, even in the presence of Srebf1-overexpres
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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