Del-1 Modulation in Inflammation and Bone Remodeling
Summary
Del-1 is a multifunctional secreted protein that balances inflammatory responses and bone homeostasis. Initially characterised as an anti-inflammatory endothelial factor, Del-1 controls neutrophil recruitment by antagonising integrin-mediated adhesion. Beyond its immune-regulatory role, Del-1 acts directly on bone cells to promote osteoblast differentiation and inhibit osteoclast formation, thereby supporting bone formation and remodelling. In inflammatory conditions such as periodontitis or age-related bone loss, Del-1 expression is downregulated, leading to excessive bone resorption and impaired regeneration. Restoration of Del-1 levels through pharmacological agents, including macrolide antibiotics, or via exogenous delivery has been shown to regenerate bone and resolve inflammation. Mechanistic studies have elucidated Del-1 signalling pathways involving integrin β3-FAK-ERK1/2-RUNX2 activation in osteoprogenitors, as well as its interaction with growth factor and cytokine networks. Collectively, these findings position Del-1 as a global regulator of the inflammation–bone remodelling axis with promising therapeutic applications in inflammatory bone disorders, fracture healing and regenerative medicine.
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Del-1 Modulation in Inflammation and Bone Remodeling publication trend
The graph below shows the total number of articles in del-1 modulation in inflammation and bone remodeling across all publications each year (not limited to Nature Index journals).
Technical terms
Del-1 (Developmental Endothelial Locus-1): a secreted glycoprotein that limits neutrophil adhesion and promotes bone formation by activating integrin-mediated signalling in osteoprogenitors.
Osteoblast differentiation: the process by which mesenchymal progenitor cells mature into bone-forming osteoblasts capable of producing mineralised matrix.
Osteoclastogenesis: the formation and activation of osteoclasts, the multinucleated cells responsible for bone resorption during remodelling and inflammatory bone loss.
BCSPs (Bone, Cartilage, Stromal Progenitors): transit-amplifying progenitor cells derived from skeletal stem cells that expand to support bone repair and regeneration.
Macrolide antibiotics: a class of antimicrobials, such as erythromycin, that possess secondary immunomodulatory effects including upregulation of Del-1.
References
- Erythromycin Restores Osteoblast Differentiation and Osteogenesis Suppressed by Porphyromonas gingivalis Lipopolysaccharide. Pharmaceuticals (2023).
- Del1 Is a Growth Factor for Skeletal Progenitor Cells in the Fracture Callus. Biomolecules (2023).
- A novel macrolide–Del-1 axis to regenerate bone in old age. iScience (2024).
- The secreted protein DEL-1 activates a β3 integrin–FAK–ERK1/2–RUNX2 pathway and promotes osteogenic differentiation and bone regeneration. Journal of Biological Chemistry (2020).
- Expression and Function of the Homeostatic Molecule Del‐1 in Endothelial Cells and the Periodontal Tissue. Journal of Immunology Research (2013).
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