Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Pulsed electromagnetic field drives osteogenic and suppresses adipogenic differentiation of bone marrow mesenchymal stem cells via Wnt/β-catenin signaling to ameliorate osteoporosis.

Wei J., He Z., Xie J., Xu F.

Animal Study, published in Bone Rep (2026) — 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
Bone Rep (2026)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
42100710
DOI
10.1016/j.bonr.2026.101920

Abstract (original English)

A pathological shift in bone marrow mesenchymal stem cell (BMSC) differentiation towards adipogenesis at the expense of osteogenesis is a key cellular driver of osteoporosis induced by glucocorticoids or estrogen deficiency. Pulsed electromagnetic field (PEMF) therapy shows clinical promise for bone disorders, yet its capacity to directly correct this lineage imbalance and the specific molecular mechanisms involved remain insufficiently defined. Here, we demonstrate that PEMF (75 Hz, 1.5 mT) directly counteracts dexamethasone (Dex)-induced effects in rat BMSCs, promoting osteogenic differentiation and concurrently suppressing adipogenesis in vitro . Mechanistically, PEMF activates the canonical Wnt/β-catenin pathway, evidenced by β-catenin nuclear translocation and upregulation of target genes (Axin2, LEF-1). The functional necessity of this pathway was confirmed using the pharmacological inhibitor XAV-939, which completely abrogated PEMF's pro-osteogenic and anti-adipogenic effects. In ovariectomized (OVX) rats, daily PEMF exposure for 8 weeks significantly preserved trabecular bone mass and microarchitecture, enhanced bone formation rate, and reduced bone marrow adiposity. Critically, in vivo co-administration of XAV-939 markedly attenuated these therapeutic benefits. Our findings establish that PEMF ameliorates osteoporosis by acting as a physical activator of the Wnt/β-cate

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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