ArticleCellular and molecular life sciences : CMLS2024
EEF1B2 regulates bone marrow-derived mesenchymal stem cells bone-fat balance via Wnt/β-catenin signaling.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Rapid mineralization of hydrothermally induced TiOJournal of materials science. Materials in medicine · 2026Article
- Pulsed electromagnetic field drives osteogenic and suppresses adipogenic differentiation of bone marrow mesenchymal stem cellsBone reports · 2026Article
- Fabrication of Fructooligosaccharide-Food science & nutrition · 2026Article
- Case Report: Cortical bone loss, impaired mineralization, and reduced adiposity contributing to chronic bone pain in SFRP4-related skeletal disease with an ALPL variant.Frontiers in endocrinology · 2026Article
- Bidirectional regulation factor of bone marrow mesenchymal stromal cells differentiation: a focus on bone-fat balance in osteoporosis.Stem cell research & therapy · 2025Review
- Preliminary Exploration of the Osteogenic Differentiation Mechanism of Bone Marrow Mesenchymal Stem Cells Regulated by SYVN1.Journal of musculoskeletal & neuronal interactions · 2025Article
- Role of histone-lysine N-methyltransferase 2D (KMT2D) in MEK-ERK signaling-mediated epigenetic regulation: a phosphoproteomics perspective.Frontiers in bioinformatics · 2025Article
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Abstract
The pathological advancement of osteoporosis is caused by the uneven development of bone marrow-derived mesenchymal stem cells (BMSCs) in terms of osteogenesis and adipogenesis. While the role of EEF1B2 in intellectual disability and tumorigenesis is well established, its function in the bone-fat switch of BMSCs is still largely unexplored. During the process of osteogenic differentiation, we observed an increase in the expression of EEF1B2, while a decrease in its expression was noted during adipogenesis. Suppression of EEF1B2 hindered the process of osteogenic differentiation and mineralization while promoting adipogenic differentiation. On the contrary, overexpression of EEF1B2 enhanced osteogenesis and strongly inhibited adipogenesis. Furthermore, the excessive expression of EEF1B2 in the tibias has the potential to mitigate bone loss and decrease marrow adiposity in mice with osteoporosis. In terms of mechanism, the suppression of β-catenin activity occurred when EEF1B2 function was suppressed during osteogenesis. Our collective findings indicate that EEF1B2 functions as a regulator, influencing the differentiation of BMSCs and maintaining a balance between bone and fat. Our finding highlights its potential as a therapeutic target for diseases related to bone metabolism.
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