2004 Volume 15 Issue 4 Pages 277-285
Angiogenesis is an essential process in not only the development of tissue/organ but also the tissue remodeling following tissue injuries-inflammation. On the other hand, angiogenesis can participate in the acceleration of basic diseases in angiogenic diseases. In fact, angiogenesis participates in the progression of atherosclerosis, which is the major cause of ischemic diseases in human organs, especially in heart, brain and lower extremities. Therefore, therapeutic angiogenesis can act the bi-directional functions in the promotion of atherogenesis itself besides the rescue of ischemic organs, as a two-edged sword in patients with atheroslcerotic diseases. In this paper, the mechanism of FGF-2-induced angiogenesis in ischemic limb animal models is reviewed, and FGF-2 gene transfer using SeV has been shown to be an effective therapeutic tool for ischemic tissue/organ, on the basis of FGF-2-induced hierarchical and harmonized angiogenesis with other endogeneous angiogenic factors such as VEGF-A, -C, HGF and PDGF, which would be expressed by endothelial cells, smooth muscle cells/pericytes and fibroblastsHowever, the FGF-2- induced effects on exogeneous and endogeneous expression of angiogenic factors are limited to be local but not systemic. From these findings, the FGF-2 gene transfer using SeV can be a novel and effective therapeutic tool for ischemic atherosclerotic diseases to develop functional collateral vessels.
