5. Conclusion
Based on these knowledge, aspirin is an intriguing and promising antiangiogenesis agent. We have addressed here the some potential antiangiogenic effects of aspirin therapy in not only decreasing endothelial cell proliferation and migration, but also in reducing macrophage or platelet-mediated angiogenesis. We have also discussed some mechanisms through which aspirin treatment may normalise existing blood vessels, including preventing disintegration of endothelial adheren junctions and recruiting pericytes, thereby reducing permeability and leakiness through endothelial cell layer. When a single-molecule is blocked, the tumor may bypass this angiogenic protein through overexpression of other angiogenic factors, resulting in a low therapeutic effect. The above drawback may be overcome by aspirin inhibiting several angiogenic molecules simultaneously, such as VEGF, cyclooxygenase, matrix metalloproteinase, and heparanase. Furthermore, more clinical trials are needed to validate the antiangiogenic mechanisms and benefits of aspirin therapy, especially in combination with existing chemotherapies to prevent various human tumors, such as glioblastoma, breast cancer and colorectal cancer. However, angiogenesis is essential for reproductive function and wound healing, so the dose of aspirin should be quantified to inhibit tumor angiogenesis, but it does not injure healthy endothelial function and maintenance. The novel derivatives could be designed from aspirin backbone to be more antiangiogenic and more suitable as an antiangiogenesis agent while overcoming the side effects of aspirin.