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Angiogenesis is the physiological process through which new blood vessels form from pre-existing ones, essential for normal development, wound healing, and tissue repair [1, 5, 6]. It is distinct from vasculogenesis, which involves the de novo formation of vessels from endothelial progenitor cells during early development [6, 11]. In healthy adults, this process is generally quiescent but can be rapidly activated by a balance of pro-angiogenic factors, such as Vascular Endothelial Growth Factor (VEGF), and various anti-angiogenic inhibitors [1, 5, 6]. Pathological angiogenesis is a critical driver of various diseases, particularly cancer, where it allows tumors to establish a dedicated nutrient supply to facilitate growth and metastasis [1, 2, 5]. Beyond oncology, abnormal vessel formation contributes to inflammatory disorders like rheumatoid arthritis and ocular conditions such as age-related macular degeneration and diabetic retinopathy [5, 11]. Therapeutic strategies primarily focus on inhibiting this process using monoclonal antibodies or small-molecule kinase inhibitors to starve tumors, though pro-angiogenic therapies are also investigated for treating ischemic heart and limb diseases [1, 4, 10].
Drugs targeting this process typically act as anti-angiogenic agents by neutralizing pro-angiogenic ligands (such as VEGF) or by blocking their cognate receptor tyrosine kinases (such as VEGFR2), thereby inhibiting the signaling cascades that drive endothelial cell activation, proliferation, and migration.
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