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Also, after an encouraging report about a positive correlation between MVD and cerebrospinal uid FGF in children with brain tumors, FGF levels in body uids do not always reect tumor vascularity.Moreover, serum FGF may not entirely derive from the neoplastic tissue in cancer patients. Moreover, osmotic shock and shear stress induce the release of FGF from endothelial cells. The inammatory response may also cause cell damage, uid and plasma protein exudation, and hypoxia.Endothelial cell damage results in increased FGF Tafamidis production and release; exudated brin; hypoxia upregulates the production of angiogenic growth factor, including VEGF. Furthermore, hypoxia increases endothelial cell responsiveness to FGF by promoting HSPG synthesis. Conversely, by interacting with endothelial cells, FGF may amplify the inammatory and angiogenic response by inducing vasoactive effects and the recruitment of an inammatory inltrate. Indeed, FGF, but not FGF, causes vasodilation of coronary arterioles via an increase in NO production. Moreover, FGF exerts a direct chemotactic effect on monocytes. Consequently, polymorphonuclear leukocyte adhesion and transendothelial migration are reduced. Similarly, monocytemacrophages adhesion to endothelium and the chemotactic response to various chemokines are markedly inhibited by longterm stimulation by FGF or FGF, but not by VEGF and tissue factor expression in endothelial cells. Different delivery methods, including intravenous, intracoronary, intramyocardial and intrapericardial routes, are normally used to administer angiogenic factors either as recombinant proteins or by gene transfer using naked DNA or vectors that encode the gene to be incorporated into the target cells.Among the different members of the FGF family, FGF, FGF, FGF, and FGF have been more widely investigated, with particular emphasis to FGF.For instance, in swine and canine models of coronary occlusion, intracoronary FGF Silodosin administration or local injection in the myocardium can reduce scar size, preserve myocardial function, and increase number of blood vessels. In CAD patients, slowrelease FGF capsules implanted in the myocardium in a phase I clinical trial caused a signicant reduction in size of the ischemic region and treated patients had more freedom from angina recurrence than controls. Also, singlebolus intracoronary FGF infusion showed transient benecial effects, including reduction of angina symptoms, increase of treadmill tolerance and quality of life. Transient benecial effects were observed also in the phase II trial FIRST in which FGF was administered via intracoronary infusion. In PAD patients, a positive response was observed in a phase I trial in which patients with symptoms of claudications and advanced peripheral arterial disease where given intraarterial FGF infusion. Indeed, administration of a FGF mutant with prolonged halflife showed an augmentation of blood ow and function in ischemic porcine myocardium. Similar benecial effects were observed in a hindlimb ischemia rabbit model using a single intramuscolar dose of naked DNA encoding FGF. Phase I clinical trials have shown some benecial effects following FGF protein injection in ischemic myocardium. Similarly, intramuscular FGF gene injection in PAD patients resulted in a transient benecial effect that was not sustained at months. The angiogenic potency of FGF and FGF was evaluated by gene therapy using an adenoviral vector in the rabbit hindlimb. However, further investigation is required to solve mayor problems that are critical to successful therapy: identication of the most effective delivery approach, proper selection of patients, timing and dosage of angiogenic factors used alone or in combinations.

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