Angiogenesis pathways in endothelial cells

Angiogenesis pathways in endothelial cells refer to the integrated signaling networks that drive the formation of new blood vessels from existing vasculature. This process is primarily governed by the Vascular Endothelial Growth Factor (VEGF) family and its receptors (VEGFR1, VEGFR2, and VEGFR3), which trigger downstream cascades like the PI3K/Akt and MAPK/ERK pathways to promote endothelial cell survival, proliferation, and migration [1, 2, 5]. Other essential pathways include the Notch signaling system, which coordinates the differentiation of tip and stalk cells during vessel sprouting, and the Angiopoietin-Tie2 axis, which regulates vascular stability and maturation [2, 4]. In pathological conditions such as cancer and wet age-related macular degeneration, these pathways are hijacked or over-activated, leading to excessive and disorganized vessel growth that supports tumor progression or vision loss [1, 9]. Therapeutic strategies targeting these pathways, such as monoclonal antibodies like bevacizumab and small-molecule tyrosine kinase inhibitors like sunitinib, have become cornerstones of treatment in oncology and ophthalmology [5, 9]. However, clinical use is often limited by the development of drug resistance and systemic side effects, including hypertension, proteinuria, and impaired wound healing [1, 5].

Other names

Angiogenic signalingEndothelial cell angiogenesisVEGF/VEGFR signaling pathwayTumor angiogenesis pathwaysNeovascularization pathways

Inhibition of pro-angiogenic signaling cascades, primarily the VEGF-VEGFR axis, to suppress endothelial cell activation, proliferation, and migration, thereby preventing the formation of new blood vessels.