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. Author manuscript; available in PMC: 2015 Jun 1.
Published in final edited form as: Int J Biochem Cell Biol. 2014 Apr 6;51:89–92. doi: 10.1016/j.biocel.2014.03.029

Figure 1.

Figure 1

Figure 1

Cellular mechanisms regulating steady-state and (chronic) stress erythropoiesis. In steady-state erythropoiesis, erythroid proliferation, differentiation and survival is primarily dependent on EpoR/Jak2/Stat5 signaling and iron-dependent IRE/IRP modulation (A). In (chronic) stress erythropoiesis, the expansion of stress erythroid progenitors is regulated by several other mechanisms in addition to the EpoR/Jak2/Stat5 pathway. This includes BMP4 signaling through SMAD4 and SCF/c-kit signaling through Akt/Erk, which are both dependent on oxygenation, possibly via HIFs; pIgA1-mediated transferrin receptor 1 (TfR1) activation which stimulates Akt/Erk and potentiates EpoR/Stat5 signaling; glucocorticoid receptor (GR) signaling via ZFP36L2; and the desert Hedgehog (Dhh) pathway, which inhibits the response. Moreover, there is a regulating role of the microenvironment through Notch2 signaling, which stimulates switching of early progenitors towards the erythroid lineage, as well as macrophage-associated regulation, which stimulate erythropoiesis through a currently unknown mechanism (B).