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Endothelial cell angiogenesis is the fundamental biological process through which new blood vessels are formed from pre-existing ones, primarily driven by the activation, proliferation, and migration of endothelial cells [3, 4]. Under normal physiological conditions, it is essential for embryonic development, wound repair, and the female reproductive cycle, but it is tightly regulated by a balance of pro- and anti-angiogenic factors [3, 6]. Pathologically, it is a key driver of tumor growth and metastasis, as tumors stimulate persistent neovascularization to provide oxygen and nutrients [1, 4]. This process also plays a significant role in blinding ocular diseases like age-related macular degeneration and diabetic retinopathy, where leaky, fragile new vessels cause significant tissue damage [4, 5]. Therapeutic strategies focus on inhibiting this process, primarily by targeting the vascular endothelial growth factor (VEGF) pathway using monoclonal antibodies like bevacizumab or multi-kinase inhibitors like sunitinib [1, 7]. These drugs act by preventing the signaling cascade that triggers endothelial cell growth and survival, effectively 'starving' tumors or reducing pathological vessel formation in neovascular diseases [1, 4].
Inhibition of the vascular endothelial growth factor (VEGF) signaling pathway, either by sequestering pro-angiogenic ligands or by blocking the intracellular kinase activity of receptors such as VEGFR-2, thereby preventing endothelial cell activation, proliferation, and subsequent vessel formation.
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