Loss of VEGF-C or VEGFR3 function or gain of VE-cadherin function causes identical defects in sinusoidal and lymphatic growth, resulting in anemia and lymphedema. Mechanistically, VEGF-C drives VE-cadherin phosphorylation and endocytosis whereas VE-cadherin prevents VEGFR3 internalization and downstream growth factor signaling. In the absence of VEGFR3, reducing VE-cadherin levels rescues vascular growth by potentiating VEGF-C–VEGFR2 signaling.
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This is a summary of: Sung, D. C. et al. Sinusoidal and lymphatic vessel growth are controlled by reciprocal VEGF-C–CDH5 inhibition. Nat. Cardiovas. Res. https://doi.org/10.1038/s44161-022-00147-0 (2022).
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VEGF signaling and cell adhesion interplay controls sinusoidal and lymphatic growth. Nat Cardiovasc Res 1, 986–987 (2022). https://doi.org/10.1038/s44161-022-00152-3
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DOI: https://doi.org/10.1038/s44161-022-00152-3