It has been shown that ASCs mediate cardioprotection by producing and releasing soluble mediators with known cytoprotective properties. Most of these factors act through the activation of the pro-survival PI-3 kinase/Akt pathway. Factors like FGF-2 and EPO can activate the protein kinase C pathway, which has been shown to mediate cardioprotection. Interleukin 11 (IL11) also activates survival signalling cascades in PI3K/Akt and ERK1/2-STAT3 dependent fashion. The mechanisms of action through which Sfrp2 and TB4 lead to cardioprotection are partially undetermined and need to be further clarified. Finally, other factors and pathways are certainly involved but are still unidentified. Abbreviations: IL11, interleukin 11; HGF, hepatocyte growth factor; IGF-1, insulin growth factor 1; VEGF, vascular endothelial growth factor; EPO, erythropoietin; FGF-2, fibroblast growth factor-2; TB4, thymosin beta 4; GF, growth factor; C, cytochrome c; GLUT, glucose transporter; VDAC, voltage-dependent anion channel.