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Angiogenesis-related signaling refers to the complex network of biochemical pathways that regulate the formation of new blood vessels from pre-existing ones. This process is primarily driven by pro-angiogenic factors such as vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and angiopoietins, which bind to their respective tyrosine kinase receptors on endothelial cells [1, 2]. Activation of these receptors triggers downstream intracellular cascades, including the PI3K/Akt and MAPK/ERK pathways, which promote endothelial cell survival, proliferation, and migration [2, 6]. In pathological conditions like cancer, the 'angiogenic switch' is constitutively activated, allowing tumors to establish a blood supply for growth and metastasis [4, 12]. Therapeutic targeting of these signaling pathways, particularly through VEGF/VEGFR inhibitors like bevacizumab and sunitinib, has become a cornerstone in treating various malignancies and ocular diseases [1, 7]. However, challenges such as drug resistance and off-target effects like hypertension and impaired wound healing remain significant concerns in clinical practice [1, 7]. Beyond oncology, modulating these pathways is also explored for treating ischemic diseases and inflammatory conditions [8, 11].
Inhibition of pro-angiogenic growth factors and their receptors to disrupt endothelial cell proliferation and migration.
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