Fig. 6: A proposed model for the role of Sema7A in EndMT.

When exposed to d-flow, endothelial Sema7A expression is upregulated, potentially by the cAMP/CREB (cAMP response element-binding protein) pathway. Endothelial Sema7A upregulates the transcription factor ATF3 through interaction with β1 integrin, leading to TGF-β2 transcription, and activation of TGF/Smad3 signaling pathway, and thus inducing EndMT.