FKBP5 promotes osteogenic differentiation of mesenchymal stem cells through type-I interferon pathway Inhibition
Tang J., Li M., Chen Y., Liang Y., Yan W., Ning Q.
Animal Study, published in Cell Mol Life Sci (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
- Cell Mol Life Sci (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 40515831
- PMCID
- PMC12167206
- DOI
- 10.1007/s00018-025-05754-1
- Citations
- 4
Abstract (original English)
The decreased osteogenesis of bone marrow mesenchymal stem cells (BMSCs) is an important factor causing bone loss. Nevertheless, its deep molecular mechanism has still not been fully clarified. To elucidate the regulatory mechanisms underlying BMSC osteogenesis, we conducted a bioinformatics screen using public datasets from the Gene Expression Omnibus (GEO) database to identify genes displaying significant expression dynamics during the osteogenic differentiation of BMSCs. We observed a significant upregulation of FK506 Binding Protein 5 (FKBP5) expression during the osteogenic differentiation of BMSCs. Besides, knockdown and overexpression of FKBP5 could reduce and increase osteogenic markers and Alizarin Red S (ARS) staining, respectively. Enrichment analysis of RNA sequencing (RNA-seq) demonstrated that downregulation of FKBP5 activated IFNα/β signaling pathway. FKBP5 overexpression relieved the inhibitory effect of IFNβ on osteogenesis. In addition, one of the upregulated interferon-stimulated genes (ISG), interferon-induced protein with tetratricopeptide repeats 2 (IFIT2), negatively regulated osteogenesis of BMSCs. IFIT2 knockdown rescued negative effect on osteogenesis caused by downregulation of FKBP5. Hydroxyapatite scaffold implanted in nude mice and drilled tibiae model in C57BL/6 mice confirmed positive role of FKBP5 in osteogenesis in vivo. Therefore, we determine
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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