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Angiogenic blood vessel endothelial cells are a specialized population of endothelial cells that undergo active proliferation, migration, and tube formation to create new blood vessels from pre-existing ones, a process known as angiogenesis. In healthy adults, this process is largely quiescent, occurring primarily during wound healing and the female reproductive cycle. However, in pathological conditions such as cancer, these cells are switched on by pro-angiogenic factors like VEGF and FGF secreted by tumor cells or the microenvironment, leading to the formation of a disorganized and leaky vascular network that supports tumor growth and metastasis. Therapeutic strategies targeting these cells aim to starve the tumor of oxygen and nutrients or to normalize the vasculature to improve the delivery of other treatments. Common pharmacological approaches include neutralizing circulating growth factors like VEGF or inhibiting their cognate receptors, such as VEGFR2, on the endothelial cell surface using monoclonal antibodies or small-molecule tyrosine kinase inhibitors. While effective in various solid tumors, these therapies are often associated with class-specific toxicities such as hypertension and impaired wound healing due to the systemic inhibition of physiological angiogenesis.
Inhibition of pro-angiogenic signaling pathways, primarily the VEGF/VEGFR axis, to suppress endothelial cell proliferation, migration, and survival, thereby disrupting the formation of new blood vessels.
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