A model for G-CSF–induced mobilization by FGF-23 from erythroblasts. G-CSF or activation of the sympathetic nervous system, inducing hypoxia, increases the expression and release of FGF-23, mainly from erythroblasts (and also partially from stromal cells). Homeostatic mechanisms that contribute to HSPC anchoring to the microenvironment, such as chemoattraction toward CXCL12-abundant reticular (CAR) cells, are suppressed by the high concentration of bone marrow (BM) FGF-23, which counteracts the CXCR4 function via FGFRs. HSC, hematopoietic stem cell; SNS, sympathetic nervous system. See Figure 7 in the article by Ishii et al that begins on page 1457.

A model for G-CSF–induced mobilization by FGF-23 from erythroblasts. G-CSF or activation of the sympathetic nervous system, inducing hypoxia, increases the expression and release of FGF-23, mainly from erythroblasts (and also partially from stromal cells). Homeostatic mechanisms that contribute to HSPC anchoring to the microenvironment, such as chemoattraction toward CXCL12-abundant reticular (CAR) cells, are suppressed by the high concentration of bone marrow (BM) FGF-23, which counteracts the CXCR4 function via FGFRs. HSC, hematopoietic stem cell; SNS, sympathetic nervous system. See Figure 7 in the article by Ishii et al that begins on page 1457.

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