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The promotion of angiogenesis via the secretion of growth factors such as Vascular Endothelial Growth Factor (VEGF) and Fibroblast Growth Factor (FGF) is a fundamental biological process involving the formation of new blood vessels from pre-existing ones (Source: NIH). In physiological conditions, this mechanism is essential for embryonic development, the female reproductive cycle, and tissue repair following injury. However, in pathological states like cancer, tumors exploit this process by secreting high levels of these factors to establish a vascular network that provides nutrients and oxygen, thereby facilitating tumor growth and metastatic spread (Source: PubMed). In ophthalmology, the overproduction of VEGF is a primary driver of neovascularization in wet age-related macular degeneration and diabetic retinopathy. Therapeutic interventions typically involve monoclonal antibodies that sequester the ligands or small-molecule inhibitors that block the intracellular kinase domains of their respective receptors, VEGFR and FGFR (Source: StatPearls). While effective in slowing disease progression, these therapies are associated with systemic side effects such as hypertension and impaired wound healing due to the inhibition of basal angiogenic signaling.
Inhibition of growth factor binding to receptor tyrosine kinases (VEGFR and FGFR) using monoclonal antibodies or decoy receptors, or direct inhibition of the intracellular tyrosine kinase domain to prevent downstream signaling pathways like MAPK/ERK and PI3K/Akt.
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