Fig. 9: Regulation of endovascular progenitors cell fate.

The fate of EVPs is maintained by the co-inhibitory relationship between SOX9 and RBPJ maintained in a progenitor state in homoeostasis. However, increased expression of SOX9, either through the loss of RBPJ, or activation of the hedgehog pathway results in the translation of SNAIL and SLUG, driving the expression of mesenchymal-related factors such as FSP1, αSMA and PDGFRA. Thus, triggering EndMT and excessive scar formation. Conversely, the deletion of SOX9 promotes Notch signalling and RBPJ activities, favouring endothelial differentiation and vascularisation.