Celastrol regulates bone marrow mesenchymal stem cell fate and bone-fat balance in osteoporosis and skeletal aging by inducing PGC-1α signaling.
Li L., Wang B., Li Y., Li L., Dai Y., Lv G.
Laboratory Study, published in Aging (Albany NY) (2020) — 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
- Laboratory Study
- Journal
- Aging (Albany NY) (2020)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 32723973
- PMCID
- PMC7521495
- DOI
- 10.18632/aging.103590
- Citations
- 13
Abstract (original English)
Celastrol has recently been identified as a prospective new treatment for obesity and several metabolic complications. However, the effect of Celastrol in osteoporosis (OP) remains unknown. In this study, we demonstrated that Celastrol promotes osteoblast differentiation and prevents adipocyte differentiation in bone marrow mesenchymal stem cells (BM-MSCs) in vitro . Mechanistically, Celastrol was able to control the differentiation of BM-MSCs by stimulating PGC-1α signaling. Moreover, administration of Celastrol could alleviate bone loss and bone marrow adipose tissue (MAT) accumulation in ovariectomized (OVX) mice and aged mice. Together, these results recommended that Celastrol could regulate BM-MSCs fate and bone-fat balance in OP and skeletal aging by stimulating PGC-1α, which might act as a possible therapeutic target for OP and for the prevention of skeletal 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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