Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

Apoptotic vesicles rectify senile bone-fat imbalance by activating Thy1-ERK-TAZ axis.

Jiang Y., She J., Wang Z., Zhu Y., Liu Y., Zhang P.

Animal Study on Systemic / IV, published in J Nanobiotechnology (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
Read the A–D evidence level guide

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 Nanobiotechnology (2025)
Country
England
Reported sample size
—
Source database
PubMed
PMID
41390652
PMCID
PMC12817589
DOI
10.1186/s12951-025-03928-4
Citations
1

Abstract (original English)

Background Senile bone-fat imbalance poses a significant public health burden in aging populations. This study investigates how aging affects the heterogeneity of mesenchymal stem cell (MSC)-derived apoptotic vesicles (apoVs) and develops a therapeutic strategy to rectify age-related bone-fat metabolic disorders. Results Protein cargo analysis revealed that MSC-derived apoVs undergo age-dependent compositional remodeling, with Thy1 identified as a key biomarker progressively declining with donor aging. Functional validation confirmed Thy1's critical role in mediating apoV osteoinductive and anti-adipogenic capacities. Engineered Thy1-enriched apoVs, produced through magnetic-activated sorting and protein corona technology, significantly enhanced osteogenesis and suppressed adipogenesis in recipient MSCs by activating the Thy1-ERK-TAZ signaling axis. In aged mouse models, these engineered apoVs restored trabecular bone mass, reduced marrow adipose tissue, and ameliorated systemic lipid metabolism disorders. Conclusions This work establishes Thy1 as a functional biomarker for aging-related apoV heterogeneity and demonstrates that engineered Thy1-enriched apoVs represent a clinically scalable therapeutic approach for senile bone-fat imbalance. The identified Thy1-ERK-TAZ mechanism provides a tunable platform for developing extracellular vesicle-based interventions against age-rela

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
AnimalsMiceMesenchymal Stem CellsOsteogenesisApoptosisAdipogenesisExtracellular VesiclesThy-1 AntigensBone and BonesHumans

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