Vascular endothelial growth factor and basic fibroblast growth factor signaling complexes (VEGF/bFGF signaling complexes)

The Vascular Endothelial Growth Factor (VEGF) and basic Fibroblast Growth Factor (bFGF) signaling complexes are essential mediators of angiogenesis and mesenchymal cell proliferation [PubMed: 10449143]. VEGF signaling, primarily through VEGFR2, is the dominant driver of endothelial cell migration and tube formation, while bFGF (FGF2) acts as a potent mitogen that can stimulate angiogenesis independently or synergistically with VEGF [PubMed: 15156179]. These pathways are frequently co-opted by tumors to establish a robust blood supply, and bFGF signaling often serves as a bypass mechanism for tumors to escape anti-VEGF therapies [PubMed: 22392911]. In addition to cancer, these complexes play roles in ocular diseases like wet age-related macular degeneration and various inflammatory conditions [PubMed: 17067916]. Pharmacological targeting of these complexes typically involves multi-kinase inhibitors that block the intracellular tyrosine kinase domains of both VEGFR and FGFR families [PubMed: 25135130]. Dual inhibition is designed to provide more comprehensive suppression of tumor vascularization and overcome the limitations of monotherapy [PubMed: 21934310]. Common side effects of targeting these pathways include hypertension, proteinuria, and impaired wound healing due to the systemic inhibition of physiological vessel maintenance [PubMed: 19139177].

Other names

VEGF/FGF2 signalingVEGFR/FGFR signaling pathwaysAngiogenic growth factor signalingVascular endothelial growth factor and fibroblast growth factor 2 signaling

Competitive inhibition of ATP binding to the intracellular tyrosine kinase domains of VEGFR and FGFR receptors, preventing downstream signaling cascades such as MAPK/ERK and PI3K/Akt; Neutralization of circulating VEGF and bFGF ligands.