In the last few years, we have been deluged with information on ang- genesis. Scientists and the public at large are exposed daily to this “new” science, not just in specialist journals and texts, but in the tabloid press, where popular articles refer to angiogenic therapies as magic bullets and miracle cures for cancer, arthritis, retinopathies, heart disease, and circulatory problems. Is there no ill this approach will not cure? The fact that so much time, effort, and resource have been and continue to be dedicated to this new science is clear testament to its importance. Yet many fundamental aspects of angiogenesis remain poorly und- stood, in particular cues that activate the process. This fact has to some extent been masked behind a surfeit of fine detail; we can’t see the wood for the trees. Most studies of angiogenesis identify single links in a long chain of events. Furthermore, each study is itself hampered by the limitations of the biological end-point chosen. For instance, though endothelial proliferation may well be necessary for angiogenesis, it is not sufficient. Therefore, measuring endothelial proliferation in response to a novel growth factor, and on the basis of this obs- vation, stating that the factor is “angiogenic,” is unsound logic. It is important that researchers in this field, and perhaps more importantly those experimenting at its periphery, recognize the limitations of their chosen biological end-points.
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