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Neovascularization is the process by which new blood vessels are formed from existing vasculature through proliferation and migration of endothelial cells[1][2]. It is a normal component of embryonic development, wound healing, and tissue repair. However, pathological neovascularization underlies many disease states, including tumor progression, age-related macular degeneration, proliferative diabetic retinopathy, and inflammatory eye diseases[1][3][4]. Pathological neovascularization is driven mainly by local upregulation of pro-angiogenic factors, most importantly vascular endothelial growth factor (VEGF), as well as fibroblast growth factors (FGFs), platelet-derived growth factor (PDGF), and others[1][3]. New vessels in diseases such as cancer or eye disease are typically abnormal, contributing to hypoxia, leaky vasculature, tissue edema, and disease complications[1][3][4]. While therapeutic targeting of specific molecules (e.g., VEGF and its receptors) involved in the neovascularization process is a validated strategy for some diseases (such as anti-VEGF therapy in cancer and retinal diseases), "neovascularization process" is not itself a molecular drug target. Instead, it describes a general physiological and pathological process regulated by multiple targets[1][3][4]. Safety concerns regarding therapies that target neovascularization mainly relate to complications from anti-angiogenic drugs: hypertension, impaired wound healing, bleeding risk, and, for ocular therapies, vision changes and local tissue effects[3][4]. In summary: "Neovascularization process" is a complex, multi-factorial biological process, not a single molecule or receptor, and should not be used as a canonical target name for drug discovery or pharmacological classification[1][3][4].
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