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Endothelial cell angiogenic signaling is a complex biological process and signaling network responsible for the formation of new blood vessels from pre-existing ones (Apte et al., 2019). This process is primarily mediated by the Vascular Endothelial Growth Factor (VEGF) family and their associated receptor tyrosine kinases, such as VEGFR2, which trigger endothelial cell proliferation, migration, and survival (Ferrara & Adamis, 2016). In clinical oncology and ophthalmology, this pathway is a major therapeutic focus, with drugs like bevacizumab and sunitinib designed to inhibit these signals to treat hypervascularized tumors and neovascular eye diseases (StatPearls, 2023). Because it encompasses a broad array of ligands, receptors, and intracellular transducers, it is classified as a biological pathway rather than a discrete therapeutic target (NIH, 2022). Consequently, while targeting angiogenesis is a common clinical strategy, the actual pharmacological targets are specific proteins within this signaling cascade (Chen & Cleck, 2009). Systemic inhibition of these pathways can lead to significant safety concerns, including hypertension and impaired wound healing, due to the role of angiogenesis in normal tissue maintenance (Eskens & Verweij, 2006).
Inhibition of pro-angiogenic growth factors (e.g., VEGF-A) or their cognate receptor tyrosine kinases (e.g., VEGFR2) to block downstream signaling cascades required for endothelial cell activation and new vessel formation (StatPearls, 2023).
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