Figure 1. The FGF signaling axis inhibits premature differentiation of cardiac progenitor cells by suppressing autophagy. Binding of the FGF to the FGFR activates the FGFR tyrosine kinase, which then activates the AKT and MAPK kinase pathways in a FRS2α-dependent manner, suppresses autophagy, and inhibits differentiation of cardiac progenitor cells. Disruption of FGF signaling by deletion of Frs2α, or suppression of FGFR, PtdIns3K, or MAPK kinase activity promotes autophagy and differentiation of cardiac progenitor cells. Consistently, stimulation of autophagy promotes cardiac progenitor differentiation; suppression of autophagy prevents the differentiation. Although disruption of FGF signaling suppresses cardiac progenitor proliferation, whether autophagy directly plays a role in regulating cardiac progenitor proliferation remains to be investigated.