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.