Transforming Growth Factor Beta Signaling in Bone Remodeling
Summary
Bone remodelling is a dynamic process that balances resorption and formation to preserve skeletal integrity. Transforming growth factor beta (TGF-β) comprises a family of secreted cytokines that regulate cellular proliferation, differentiation and matrix production via serine/threonine kinase receptors. Upon release from the bone matrix by osteoclastic activity, TGF-β activates both the canonical Smad2/3-mediated pathway and non-canonical cascades (including MAPK, PI3K/AKT and Rho GTPases). In early stages, TGF-β recruits and expands mesenchymal stem cells and committed osteoprogenitors, whereas in later stages it slows osteoblast maturation, thereby coordinating the coupling of bone formation to resorption. Dysregulated TGF-β signalling contributes to osteoporosis, osteoarthritis and heterotopic ossification. Advances in targeted delivery and biomaterial scaffolds have begun to harness TGF-β’s potent osteoinductive properties, offering new avenues for regenerative therapies while minimising systemic side-effects.
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Transforming Growth Factor Beta Signaling in Bone Remodeling publication trend
The graph below shows the total number of articles in transforming growth factor beta signaling in bone remodeling across all publications each year (not limited to Nature Index journals).
Technical terms
Transforming growth factor beta (TGF-β): A family of secreted cytokines that regulate cellular proliferation, differentiation and extracellular matrix production via serine/threonine kinase receptors.
Osteoblast: A bone-forming cell responsible for synthesis and mineralisation of the bone matrix.
Osteoclast: A bone-resorbing multinucleated cell that degrades mineralised matrix and releases stored growth factors.
Smad pathway: The canonical intracellular signalling cascade initiated by TGF-β receptors involving Smad2 and Smad3 proteins that translocate to the nucleus to regulate gene expression.
Non-canonical signalling: TGF-β-activated routes operating independently of Smads, such as MAPK, PI3K/AKT and Rho GTPase pathways.
Mesenchymal stem cell (MSC): A multipotent progenitor in the bone marrow that can differentiate into osteoblasts, chondrocytes and adipocytes.
Legumain: A lysosomal cysteine protease implicated in mediating TGF-β1’s inhibitory effects on osteoblast maturation.
References
- Unlocking the Secrets of Adipose Tissue: How an Obesity-Associated Secretome Promotes Osteoblast Dedifferentiation via TGF-β1 Signaling, Paving the Path to an Adipogenic Phenotype. Cells (2024).
- Legumain is a paracrine regulator of osteoblast differentiation and mediates the inhibitory effect of TGF-β1 on osteoblast maturation. Frontiers in Endocrinology (2024).
- Influence of the TGF-β Superfamily on Osteoclasts/Osteoblasts Balance in Physiological and Pathological Bone Conditions. International Journal of Molecular Sciences (2020).
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