Mechanisms of Angiogenesis (Experientia Supplementum) by Matthias Clauss, Georg Breier

By Matthias Clauss, Georg Breier

Is it a good suggestion to return from bedside to the bench? over the past decade, few subject matters encountered the sort of vast curiosity in bio- gy and medication as angiogenesis. the fantastic skill of the physique to revive blood circulate by means of induction of blood vessel development as a part of an adaptive method has alarmed physicians facing ailments within which angiogenesis is both exaggerated (as in tumors) or too sluggish (as in ischemic ailments of center and brain). no longer strangely, professional- and antiangiogenic techniques have discovered their approach into scientific trials. for example, for america, the NIH web site in early 2004 displayed 38 medical experiences regarding both professional- or antiangiogenic th- apies. Given the predicted overwhelming wealth of scientific info, the query will be requested no matter if additional exploration of organic mechanisms is needed or no matter if effects from the bedside are instructive sufficient to continue. this query relies additionally at the development of professional- and antiangiogenic medical trials. within the following, I supply a brief review approximately the various development that has been made during this box. for the reason that Judah Folkman proposed antiangiogenic tumor remedy thirty years in the past, it has turn into more and more glaring that brokers which intervene with blood vessel formation additionally block tumor development. as a result, antiangiogenic remedy has won a lot consciousness as a possible adjunct to standard c- cer remedy.

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Yet, the cyclic processes in the ovary are under endocrine control. It thus appears obvious to imply a functional relationship between the endocrine and the vascular system. Estrogens have been most extensively studied for their angiogenesis inducing capacity. Estrogens are capable to induce angiogenesis in vivo [61, 62]. Correspondingly, anti-estrogens have been shown to exert angioinhibitory activity [62]. Causal evidence for the role of estrogens for angiogenesis could be generated in estrogen receptor deficient mice in which angiogenesis can not be induced by estrogens [63].

Functional experiments to manipulate reproductive angiogenesis have been performed in laboratory animals including rats and mice [29, 30]. The four day reproductive cycle of these species is associated with an intense angiogenic burst following ovulation. The short duration of the cycle, however, makes it difficult to discern discrete phases of vessel maturation and vessel regression that follow the angiogenic phase of the ovarian cycle. More recently, manipulatory experiments in primates with VEGF neutralizing agents (VEGF antibody, VEGF trap, VEGF receptor antibody) have been performed in non-human primates [23, 31–34].

Based on the method of implementation and morphofunctional outcomes, IA can be considered to comprise three cognate processes, namely IMG, IAR and IBR. Presumably, each process is controlled by a specific program that is initiated and regulated by definite molecules, cells and hemodynamics. Information concerning the identity of these is gradually emerging. Hemodynamics Hemodynamic forces are obvious and important determinants of vascular architecture. Djonov et al. [19] demonstrated that clamping of one of the dichotomous branches of an artery in the CAM microvasculature increases blood flow and/or pressure in its counterpart with an almost immediate effect on branching morphology.

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