ArticleNature communications2025
Targeting Msx2 as a brake in the fusion fate of osteoclasts and an anabolic therapy in pre-clinical models of osteoporosis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Micellar LYTAC-engineered bionic coatings abrogate RANK-dependent osteocatabolism and boost fibrillogenesis-mimetic mineral accretion for empowering osteoporotic osseointegration.Bioactive materials · 2027Article
- Mitochondrial OXPHOS integrates immunometabolic cascade for bone regeneration via coupled ATP production and ROS homeostasis.Redox biology · 2026Article
- Medicine-food homologous bioactives in metabolic dysregulation-associated osteoporosis: a review of preclinical evidence and potential liver-bone and gut-bone actions.Chinese medicine · 2026Review
- Beyond resorption: targeting osteoclast fusion and polarization to restore balanced bone remodeling.Frontiers in pharmacology · 2026Review
- Targeting subchondral osteoporosis in osteoarthritis: biomechanical crosstalk and the therapeutic rationale for inflammatory microenvironment remodeling.Frontiers in immunology · 2026Review
- Platelet-derived growth factor-BB (PDGF-BB): pathophysiological roles and therapeutic implications in aging-related diseases.Frontiers in cell and developmental biology · 2026Review
- E3 ubiquitin ligases in bone homeostasis: from regulatory mechanisms to skeletal diseases and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
16 authors.
Funding
Abstract
Highly conserved homeobox genes are closely related to bone formation during embryogenesis, while their role in adult bone resorption remains unclear. In this study, we found that the homeobox gene MSX2 actively participates bone metabolism. Myeloid-specific Msx2 deficiency safeguards bone mass under physiological and pathological conditions. Loss of Msx2 acts as a "brake" in the fusion fate of osteoclasts, resulting in a larger population of pre-osteoclasts. Pre-osteoclasts secrete platelet-derived growth factor-BB (PDGF-BB), which promotes angiogenesis-mediated bone formation. Mechanistically, MSX2 directly binds to the vital osteoclastogenic transcription factor PU.1 and protects it from FBXW7-mediated ubiquitination degradation. Msx2 and Fbxw7 double knockout mitigated the protective effect of MSX2 deficiency on bone mass. Finally, we identified a natural compound, morusinol, that specifically destroys the combination of MSX2 and PU.1, promoting PU.1 degradation and attenuating ovariectomy-induced bone loss. Overall, our results demonstrate that targeting Msx2 is a promising anabolic therapy for osteoporosis.
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