ArticleIn vivo (Athens, Greece)
Gefitinib Facilitates Bone Fracture Healing
Article in In vivo (Athens, Greece). 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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10 authors.
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Abstract
BACKGROUND/
aimTo investigate the role of epidermal growth factor receptor (EGFR) inhibition in enhancing bone fracture healing by modulating box transcription factor 9 (SOX9) and bone metabolism. MATERIALS AND
methodsA rat femoral fracture model was used. Techniques included histological analysis, X-ray scoring, micro-computed tomography, immunohistochemistry, and biomechanical testing. Serum markers were analyzed with enzyme-linked immunosorbent assay, while quantitative real-time polymerase chain reaction and western blotting assessed molecular pathways. Metabolic changes were measured using a Seahorse analyzer. An EGFR inhibitor, gefitinib, was used to examine its impact on periosteal stem cell differentiation and metabolism.
resultsEGFR inhibition improved bone callus formation and quality, increased cartilage callus, and upregulated bone formation markers. Gefitinib enhanced oxidative phosphorylation and fatty acid oxidation, counteracting negative effects from lipid-reduced serum on osteoblastic differentiation of periosteal stem cell. SOX9 overexpression reduced the benefits of EGFR inhibition.
conclusionGefitinib enhances bone fracture healing by modulating lipid metabolism through SOX9, suggesting its potential as a therapeutic agent for improving fracture outcomes.
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