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- W2912275486 abstract "We reviewed recent literature on oxygen sensing in osteogenic cells and its contribution to development of a skeletal phenotype, the coupling of osteogenesis with angiogenesis and integration of hypoxia into canonical Wnt signaling, and opportunities to manipulate oxygen sensing to promote skeletal repair. Oxygen sensing in osteocytes can confer a high bone mass phenotype in murine models; common and unique targets of HIF-1α and HIF-2α and lineage-specific deletion of oxygen sensing machinery suggest differentia utilization and requirement of HIF-α proteins in the differentiation from mesenchymal stem cell to osteoblast to osteocyte; oxygen-dependent but HIF-α-independent signaling may contribute to observed skeletal phenotypes. Manipulating oxygen sensing machinery in osteogenic cells influences skeletal phenotype through angiogenesis-dependent and angiogenesis-independent pathways and involves HIF-1α, HIF-2α, or both proteins. Clinically, an FDA-approved iron chelator promotes angiogenesis and osteogenesis, thereby enhancing the rate of fracture repair." @default.
- W2912275486 created "2019-02-21" @default.
- W2912275486 creator A5069686409 @default.
- W2912275486 creator A5075094625 @default.
- W2912275486 date "2019-02-01" @default.
- W2912275486 modified "2023-09-24" @default.
- W2912275486 title "Hypoxia Signaling in the Skeleton: Implications for Bone Health" @default.
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- W2912275486 doi "https://doi.org/10.1007/s11914-019-00500-6" @default.
- W2912275486 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6653634" @default.
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