ArticleScientific reports2025
Molybdenum facilitates PDLSC-based bone regeneration through the JAK/STAT3 signaling pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Combining gelatin methacryloyl hydrogels with mesenchymal stem cells: A versatile approach for bone tissue engineering.Histology and histopathology · 2026Review
- JAK Inhibitor Tofacitinib Ameliorates Inflammation Response and Osteogenic Differentiation in Immune-Mediated Inflammatory Arthritis in Rats.International journal of rheumatic diseases · 2026Article
- Advancing Biomaterials Evaluation: A Human Quadruple Bone Cell Culture Reveals Molybdenum-Driven Pro-Osteogenic and Anti-osteoclastogenic Responses.ACS applied materials & interfaces · 2026Article
- Calpain-1 Potentiates Periodontal Regeneration via PHLPP1-ERK-Driven Osteogenesis in Periodontal Ligament Stem Cells.International dental journal · 2026Article
- Current state of bioceramic bone repair materials in immune regulation: a review.Frontiers of medicine · 2025Review
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Authors and funding
4 authors.
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Abstract
Bone regeneration is a critical area of research in the treatment of bone defects within clinical practice. Molybdenum (Mo) is an essential trace element for many organisms, which plays a vital role in various cellular activities, such as maintaining energy metabolism and promoting cell proliferation. However, whether Mo regulates the osteogenic differentiation of periodontal ligament stem cells (PDLSCs) and promotes bone tissue regeneration remains unknown. This study confirmed the nourishing effect of Mo on the osteogenic differentiation of PDLSCs, as evidenced by higher expression of osteogenic-related markers (OCN, BSP, OSX and RUNX2), ALP activity and mineralization ability. Moreover, through constructing compound material GelMA + PDLSC, we proved that Mo promoted PDLSC-based bone regeneration quantity and quality in rat calvarial defects. Finally, we revealed the underlying mechanism that the JAK/STAT3 signaling pathway actively participated in the Mo-enhanced osteogenic differentiation of PDLSCs. The inhibition of STAT3 diminished the benefit of Mo. Overall, our study found that Mo facilitated PDLSC-based bone regeneration through the JAK/STAT3 signaling pathway, which may shed new light on clinical bone regeneration therapeutic strategies.
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