VEGF receptor signaling and endothelial function

IUBMB Life. 2001 Jul;52(1-2):61-6. doi: 10.1080/15216540252774784.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Division
  • Cell Movement
  • Cell Survival
  • Endothelial Growth Factors / metabolism*
  • Endothelium / cytology
  • Endothelium / metabolism*
  • Humans
  • Lymphokines / metabolism*
  • Nitric Oxide / metabolism
  • Receptor Protein-Tyrosine Kinases / metabolism*
  • Receptors, Growth Factor / metabolism*
  • Receptors, Vascular Endothelial Growth Factor
  • Signal Transduction*
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors


  • Endothelial Growth Factors
  • Lymphokines
  • Receptors, Growth Factor
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors
  • Nitric Oxide
  • Receptor Protein-Tyrosine Kinases
  • Receptors, Vascular Endothelial Growth Factor