ZFP36 regulates the osteogenic differentiation of adipose-derived mesenchymal stem cells in osteoporosis by mediating KLF3 mRNA degradation.
Liu C., Yi M., Luo B., Wang M.
Animal Study, published in Sci Rep (2025) — 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
- Sci Rep (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40274995
- PMCID
- PMC12022323
- DOI
- 10.1038/s41598-025-98738-x
- Citations
- 1
Abstract (original English)
Osteoporosis is one of the most common bone-related diseases in which osteogenic differentiation plays a key role. Adipose-derived mesenchymal stem cells (ADMSCs), as one of the important sources of bone formation, can differentiate into osteoblasts under appropriate conditions. To investigate the effect and potential mechanism of ZFP36 on osteogenic differentiation of ADMSCs in osteoporosis by regulating the stability of KLF3 mRNA. In this study, an osteoporosis rat model was established by ovariectomy (OVX), and the expression level of KLF3 in bone tissue was detected by RT-qPCR and immunohistochemistry (IHC). To further investigate the effect of KLF3 gene knockdown on bone health in osteoporotic rats. In vitro, KLF3 over-expression was performed on ADMSCs, and the effect of KLF3 knockdown on osteogenic differentiation of ADMSCs was evaluated by alkaline phosphatase (ALP) activity assay and alizarin red S staining. In addition, RNA pull-down, dual luciferase reporter gene, RIP and Actinomycin D treatment were used to explore the regulatory mechanism of ZFP36-mediated KLF3 mRNA degradation in osteogenic differentiation. Finally, the effect of ZFP36 on osteogenic differentiation and its interaction with KLF3 were further verified by interfering with ZFP36/KLF3 expression in rats in vivo and in vitro. In the osteoporotic rat model, KLF3 expression was significantly downregulated
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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