Decreased expression of Ly-1 antibody reactive clone (Lyar) triggers enhanced adipogenesis of bone marrow mesenchymal stromal cells in aged bone marrow.
Shinyashiki Y., Onodera Y., Kawashima Y., Iwawaki N., Takehara T., Goto K.
Animal Study, published in PLoS One (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
- PLoS One (2026)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42201873
- DOI
- 10.1371/journal.pone.0349780
Abstract (original English)
Accumulation of adipocytes within the bone marrow is a frequently observed during aging. However, the molecular mechanisms underlying aberrant adipocyte differentiation in aged bone marrow remain largely unclear. In this study, we identified Ly-1 antibody reactive clone (Lyar) as an interacting partner of TGF-β activated kinase 1 (Tak1), a key molecule of non-canonical TGF-β signaling, through a proteomics approach, and demonstrated its involvement in the regulation of aging-related enhancement of adipogenesis. Lyar was not only implicated in the regulation of BMMSC proliferation but also may partly mediate the inhibitory effects of Bromodomain-containing protein 2 (Brd2). An age-associated decline in Lyar expression was associated with a reduction in FGF2-PI3K-Akt1 signaling activity in aged bone marrow. These findings suggest that Lyar may act as a context-dependent modulator of TGF-β signaling and may be involved in regulating proliferation and differentiation in BMMSCs. The age-related loss of Lyar may contribute to the complex mechanisms underlying enhanced adipogenesis in aged bone marrow, providing new insights into the regulation of mesenchymal stem cell fate during aging.
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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