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IUBMB Life. 2001 Jul;52(1-2):61-6.

VEGF receptor signaling and endothelial function.

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Ulm University Medical Center, Department of Internal Medicine II, Germany.


Angiogenesis, the formation of new blood vessels from preexisting ones, is a central process during normal development and during pathological repair. Vascular endothelial growth factor-A (VEGF-A) can stimulate both physiological and pathological angiogensis. VEGF-A is a ligand for the two receptor tyrosine kinases VEGFR-1 (Flt-1) and VEGFR-2 (KDR/Flk-1). Most biological functions of VEGF-A are mediated via VEGFR-2, whereas the role of VEGFR-1 is largely unknown. Activation of mitogen-activated kinase, stress-activated kinase, protein kinase C, and the Akt pathway are implicated in VEGF-A-dependent endothelial function, including cell survival, proliferation, generation of nitric oxide, and the induction of angiogenesis. Induction of metalloproteinases, activation of focal adhesion kinase and of PI3-kinase are implicated in VEGF-A-induced endothelial cell migration. The important role of nitric oxide as a mediator of endothelial function in vivo links the receptor signaling network to other biological effects.

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