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Angiogenic signaling factors comprise a diverse group of secreted proteins and their cognate receptors that collectively regulate the formation of new blood vessels from existing vasculature, a process known as angiogenesis [1, 11]. The most prominent members of this group include the vascular endothelial growth factor (VEGF) family (VEGF-A, -B, -C, -D, and PlGF), fibroblast growth factors (FGF), angiopoietins (ANGPT1, ANGPT2), and platelet-derived growth factors (PDGF) [1, 5, 8]. These factors typically function by binding to high-affinity receptor tyrosine kinases on the surface of endothelial cells, initiating intracellular signaling pathways such as PI3K/Akt, MAPK/ERK, and PLCγ that drive endothelial cell survival, proliferation, and migration [1, 3, 12]. In healthy tissues, the balance between pro-angiogenic and anti-angiogenic factors is tightly regulated; however, in pathological conditions like cancer and neovascular eye diseases, an 'angiogenic switch' occurs where pro-angiogenic factors are overexpressed [6, 11]. This leads to the development of disorganized, leaky vessels that support tumor growth and metastasis or cause vision loss [4, 12]. Therapeutic strategies targeting these factors, such as monoclonal antibodies that neutralize VEGF or small-molecule inhibitors of VEGFR signaling, have become standard treatments for various malignancies and retinal disorders [1, 5, 7].
Inhibition of angiogenic signaling through the sequestration of pro-angiogenic ligands or the blockade of their respective receptor tyrosine kinases [1, 5].
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