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Angiogenesis-related cell-surface and extracellular matrix (ECM) targets represent a broad functional class of molecules essential for the formation of new blood vessels from existing vasculature. This group includes prominent cell-surface receptors such as Vascular Endothelial Growth Factor Receptors (VEGFRs), Tie receptors, and various integrins (e.g., alpha-v beta-3), as well as ECM components like laminin and collagen that provide structural and signaling support (Carmeliet & Jain, Nature, 2011). These targets play a pivotal role in physiological processes like wound healing and the menstrual cycle, but they are also central to the progression of diseases characterized by pathological neovascularization, including solid tumors and exudative age-related macular degeneration (Ferrara & Adamis, Nature Reviews Drug Discovery, 2016). In cancer, the 'angiogenic switch' leads to the overexpression of these targets, facilitating tumor growth, metabolic exchange, and hematogenous metastasis (Hanahan & Weinberg, Cell, 2011). Therapeutic agents targeting these molecules, such as bevacizumab or ramucirumab, aim to starve tumors of their blood supply by neutralizing pro-angiogenic ligands or blocking their respective receptors (Jayson et al., Lancet, 2016). However, targeting these pathways often presents clinical challenges, including the development of resistance and systemic toxicities like hypertension and impaired wound repair (Verheul & Pinedo, Drugs Today, 2007).
Inhibition of pro-angiogenic signaling pathways by sequestering growth factors, blocking receptor-ligand interactions, or disrupting cell-extracellular matrix adhesion to prevent endothelial cell activation and vessel formation.
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