Fig. 6.

Schematic overview of the signalling events modulated by erythropoietin (EPO) in the hearts of endotoxemic wild-type mice. Activation of βcR-EpoR by EPO is associated with (a) activation of the phosphoinositide 3-kinase (PI3K)-Akt signalling pathway, which results in the inhibition of the activation of glycogen synthase kinase-3β (GSK-3β), which is known to suppress the activation of nuclear factor-κB (NFκB), resulting in a blunted expression of the NFκB-driven gene transcription of pro-inflammatory mediators such as interleukin-1β (IL-1β), and (b) activation of the PI3K-Akt signalling pathway, which results in the increased activation of endothelial nitric oxide synthase (eNOS) and thus the enhanced formation of nitric oxide (NO). The signalling steps that were analyzed in our study are highlighted in light grey.