File:A model of signalling networks regulating myogenic cell-fate..jpg

English: A. Activation of quiescent satellite cells to proliferate is induced by the upregulation of Notch ligand, Delta, on the surface of myofibers located near the injury site and on the satellite cells themselves. TGF-β/pSmad3 antagonize this process by keeping high levels of CDK inhibitors in satellite cells and the age-specific increase in pSmad3 accompanied by the decline in active Notch thus precludes satellite cell activation. B. Activated myogenic progenitor cells (progeny of satellite cells) proliferate without differentiation due to high levels of active Notch that inhibits Wnt signalling pathway. Wnt signaling may also skew the myogenic cell fate of satellite cells towards the fibroblast lineage in the early phase of the regenerative response. C. In the late stages of regeneration, differentiation of myogenic progenitor cells into fusion-competent myoblasts is induced by the up-regulation of Numb that inhibits Notch activation and thus, Wnt signalling is released to promote terminal myogenic cell fate. A representative picture of a myogenic progenitor cell that divides asymmetrically with respect to the levels of Numb is also shown in the insert. Cells with high Numb will go on to give rise to myoblasts and myotubes that replace damaged muscle; cells with low Numb continue to divide as pre-myoblast myogenic progenitors. Numb and Wnt might also re-enforce each other.