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The angiogenesis process via the VEGF pathway is a central mechanism for the formation of new blood vessels. Circulating or locally produced VEGFs bind to their respective cell surface receptors (VEGFRs) on endothelial cells, triggering receptor dimerization and autophosphorylation of tyrosine kinases. This activates downstream signaling cascades, including MAPK/ERK, PI3K/Akt, and FAK/p38 MAPK, leading to increased vascular permeability, endothelial cell proliferation, migration, and survival. This pathway is crucial in both physiological processes and pathological conditions like cancer, where it facilitates tumor growth and metastasis. Therapeutic targeting of the VEGF pathway aims to inhibit angiogenesis and suppress tumor growth, but may also affect normal tissue repair and cause side effects.
Inhibition of VEGF ligand binding to VEGFR receptors; Inhibition of VEGFR tyrosine kinase activity; Prevention of downstream signaling cascades (MAPK/ERK, PI3K/Akt, FAK/p38 MAPK); Reduction of endothelial cell proliferation, migration, and survival; Decreased vascular permeability; Suppression of tumor angiogenesis.
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