Angiogenesis and stroke.

Stroke results from focal cerebral ischemia due to occlusion of a cerebral blood vessel, usually an artery. Where ischemia is chronic or intermittent, collateral circulation may develop by enlargement of preexisting anastomotic channels or sprouting of new capillaries from existing vessels (angiogenesis). Angiogenesis has three attributes of particular interest in relation to cerebral vascular disease: 1) it is the principal mechanism by which the brain is vascularized; 2) unlike vasculogenesis, it continues in adulthood; and 3) as in other tissues, it can be induced in the CNS by hypoxia or ischemia. Vascular endothelial growth factor (VEGF) is a key mediator of angiogenesis. The angiopoietins, Ang-1 and Ang-2, and their common receptor, Tie-2 or Tek, constitute another signaling system that regulates angiogenesis, and which interacts with VEGF. Four recent studies provide evidence for the induction of angiogenesis, VEGF and VEGF receptor expression in experimental models of cerebral ischemia. Further understanding of the role of VEGF, VEGF receptors and angiogenesis in the brain's response to ischemia may have implications for prognosis and treatment in stroke.