The growth of blood vessels (a process known as angiogenesis) is essential for organ growth and repair. Blood vessels arose during evolution to carry oxygen to distant organs. Not surprisingly, these vessels are crucial for organ growth in the embryo and repair of wounded tissue in the adult. An imbalance in this process contributes to numerous malignant, inflammatory, ischaemic, infectious and immune disorders.
In the embryo, blood vessels provide the growing organs with the necessary oxygen to develop. Apart from their nutritive function, vessels also provide instructive trophic signals to promote organ morphogenesis. Blood vessels arise from endothelial precursors, which share an origin with haematopoietic progenitors. The close link between the blood and blood vascular systems remains important for angiogenesis throughout life, even in disease. These progenitors assemble into a primitive vascular labyrinth of small capillaries — a process known as vasculogenesis. 
Over the past 15 years, genetic studies in mice, zebrafish and tadpoles have provided insights into the key mechanisms and molecular players that regulate the growth of blood vessels (angiogenesis) or lymph vessels (lymphangiogenesis) in the embryo. Implications of members of the Notch family, the orphan receptor COUP-TFII,  the homeobox geneProx-1, angiopoietin, PDGF, VEGF and its homologue VEGF-C have been confirmed, among others.
The formation of vessels is a complex process, requiring a finely tuned balance between numerous stimulatory and inhibitory signals, such as integrins, angiopoietins, chemokines, junctional molecules, oxygen sensors, endogenous inhibitors and many others[1].