ArticleBone research2025
NELL2, a novel osteoinductive factor, regulates osteoblast differentiation and bone homeostasis through fibronectin 1/integrin-mediated FAK/AKT signaling.
Article in Bone research, 2025. 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.
- Reprogramming bone homeostasis: The recoupling-oriented framework of bidirectional regulation strategies for osteoporosis.iScience · 2026Review
- Dissecting Hypoxia Inducible Factor-Driven High Bone Mass Phenotype in Mice Lacking Osteocytic Von Hippel-Lindau.JBMR plus · 2026Article
- Integrated bioinformatic and experimental analyses identify Lumican as a key regulator of LIPUS-induced osteogenesis through Integrin β1/FAK/ERK signaling.Molecular biology reports · 2026Article
- Bakuchiol Ameliorates Glucocorticoid-Induced Osteoporosis by Enhancing Osteoblast Differentiation via Targeting FAT4 to Activate YAP1.Phytotherapy research : PTR · 2026Article
- rRGD3International journal of molecular sciences · 2026Article
- Anastellin: A Fibronectin-Derived Peptide Targeting the Tumor Microenvironment Through ECM Modulation.Cell biochemistry and biophysics · 2026Review
- Advanced bone-targeted nanomaterials for the systemic treatment of osteoporosis.Regenerative biomaterials · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
Neural EGFL-like 2 (NELL2) is a secreted protein known for its regulatory functions in the nervous and reproductive systems, yet its role in bone biology remains unexplored. In this study, we observed that NELL2 was diminished in the bone of aged and ovariectomized (OVX) mice, as well as in the serum of osteopenia and osteoporosis patients. In vitro loss-of-function and gain-of-function studies revealed that NELL2 facilitated osteoblast differentiation and impeded adipocyte differentiation from stromal progenitor cells. In vivo studies further demonstrated that the deletion of NELL2 in preosteoblasts resulted in decreased cancellous bone mass in mice. Mechanistically, NELL2 interacted with the FNI-type domain located at the C-terminus of Fibronectin 1 (Fn1). Moreover, we found that NELL2 activated the focal adhesion kinase (FAK)/AKT signaling pathway through Fn1/integrin β1 (ITGB1), leading to the promotion of osteogenesis and the inhibition of adipogenesis. Notably, administration of NELL2-AAV was found to ameliorate bone loss in OVX mice. These findings underscore the significant role of NELL2 in osteoblast differentiation and bone homeostasis, suggesting its potential as a therapeutic target for managing osteoporosis.
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Registered trials
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