Introduction Vascular endothelial growth factors (VEGFs) comprise of a multigene-encoded family of cytokines that display remarkable effects in different tissues including the vascular, epithelial and neuronal tissues. Such factors bind to both membrane-bound and soluble receptor isoforms that regulate the ability of these cytokines to trigger profound biochemical changes within cells, resulting in changes to metabolism, gene expression, cell proliferation, apoptosis and homeostasis. The cornerstone of this biochemical control is based on the interaction between soluble factors such as VEGFs and membrane-bound receptors such as VEGF receptor tyrosine kinases (VEGFRs). The endothelial monolayer that lines all blood vessels responds to VEGFs to regulate many aspects of vascular physiology. Dysfunction in the VEGF-A signalling pathways is implicated in a wide variety of diseases ranging from solid tumour metastasis to atherosclerosis. VEGF binding to membrane VEGFRs triggers intracellular signalling, post-translational protein modifications , trafficking and proteolysis. Temporal and spatial coordination of such events is critical for programming downstream responses by the endothelium. In this review, we have discussed the biochemical mechanisms that underlie new blood vessel sprouting mediated by VEGF-like cytokines. Conclusion The development of primary cell systems, multicellular models, organ culture and animal models, will dramatically increase our ability to understand the biochemical basis for how this important class of cytokines regulate animal physiology. Targeting such pathways directly or indirectly using humanised antibodies or small molecule inhibitors, is important for treating a wide variety of pathological states including solid tumour growth and metastasis, age-related macular degeneration and conditions involving blood vessel repair and regeneration.
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