ArticleResearch square2026
Delivery timing determines senomorphic efficacy: delayed local ruxolitinib restores macrophage polarization and rescues age-impaired bone repair.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
Impaired bone repair in aged individuals is driven by dysregulated macrophage polarization and chronic inflammaging. Early pro-inflammatory macrophage activity is indispensable for bone repair, yet its pathological persistence suppresses osteogenesis and promotes bone resorption. Here we show that localized, temporally delayed delivery of the JAK1/JAK2 inhibitor ruxolitinib (Rux) from a transitory barrier layer (TBL) bone graft coating restores macrophage phenotype switching and accelerates calvarial bone defect closure in aged female mice. Immediate Rux exposure prematurely suppresses the early pro-inflammatory gene expression profiling in aged bone marrow-derived macrophages, whereas TBL-mediated delayed release preserves this phase before driving a robust pro-reparative gene expression signature. Rux-TBL-coated grafts produced significantly greater bone formation than immediately dosed Rux grafts or no Rux grafts at nine weeks. These findings establish delivery timing as a critical determinant of senomorphic efficacy, supporting local delayed delivery over systemic administration following acute bone injury.
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