Abstract
A number of anti-angiogenesis drugs have been FDA-approved and are being used in cancer treatment, and a number of other agents are in different stages of clinical development or in preclinical evaluation. However, pharmacologic anti-angiogenesis strategies that arrest tumor progression might not be enough to eradicate tumors. Decreased anti-angiogenesis activity in single mechanism-based anti-angiogenic strategies is due to the redundancy, multiplicity, and development of compensatory mechanism by which blood vessels are remodeled. Improving anti-angiogenesis drug efficacy will require identification of broad-spectrum anti-angiogenesis targets. These strategies may have novel features, such as increased porosity, and are the result of complex interactions among endothelial cells, extracellular matrix proteins, growth factors, pericyte, and smooth muscle cells. Thus, combinations of anti-angiogenic drugs and other anticancer strategies such as chemotherapy appear essential for optimal outcome in cancer patients. This review will focus on the role of anti-angiogenesis strategies in cancer treatment.
Highlights
Angiogenesis is a normal and complex process controlled by certain biomolecules produced in the body
It is well known that in healthy cells, oxygen tension is key in the regulation of angiogenesis, and endothelial cells (ECs) and smooth muscle cells (SMCs) have various oxygen-sensing mechanisms, including oxygen-sensitive NADPH oxidases, endothelial nitric oxide synthase, and heme-oxygenases [34]
In comparison to other naturally occurring angiogenesis inhibitors such as angiostatin, endostatin, interferons, IL-1 and IL-12, tissue inhibitor of metalloproteinases, and retinoic acid [38,39,40], we previously reported that physiological concentrations of thyroid hormone are pro-angiogenic by multiple mechanisms
Summary
Angiogenesis is a normal and complex process controlled by certain biomolecules produced in the body. Steps toward angiogenesis include protease production, endothelial cell migration, and proliferation, vascular tube formation, anastomosis of newly formed tubes, synthesis of a new basement membrane, and incorporation of pericytes and smooth muscle cells (Figure 1B). Endothelial cells proliferate and migrate into the perivascular area, forming “primary sprouts” Subsequent lumenation of these primary sprouts leads to formation of capillary loops, which is followed by synthesis of a new basement membrane and blood vessel maturation to complete tube-like structures through which blood can flow [3]. In comparison with chemical signals that induce blood formation, there is another type of chemical signal known as an angiogenesis inhibitor (Table 1) These signals may systematically on several proteins that haveangiogenesis been identifiedinhibitor as angiogenic activators, including vascular endothelial disruptgrowth blood factor vessel(VEGF), formation or support removal existing.
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