Figure 3.

Targeting the VEGF-C/VEGFR3 axis by various therapeutic strategies. The binding of VEGF-C/D to VEGFR3 induces downstream signaling which mediates cell survival and lymphangiogenesis. The treatment of small molecule receptor tyrosine kinase inhibitors (TKIs) inhibits the activation of VEGF-C/D/VEGFR3 signaling. Monoclonal antibody (mAb) and receptor trap target VEGF-C, preventing its binding to VEGFR3. Monoclonal antibody or peptides targeting VEGFR3 prevent the binding of VEGF-C, resulting in the inhibition of VEGFR3 signaling.