Vascular endothelial growth factor and fibroblast growth factor receptor signaling complex (VEGFR/FGFR complex)

The bFGF/VEGF signaling complex at VEGFR/FGFR represents a critical regulatory node in tumor angiogenesis and vascular maintenance (PMID: 25132425). Vascular Endothelial Growth Factor (VEGF) and Basic Fibroblast Growth Factor (bFGF or FGF2) are potent mitogens that act synergistically on endothelial cells to promote the formation of new blood vessels (PMID: 10449300). While VEGF is the primary driver of angiogenesis, FGF signaling often serves as a key escape mechanism, leading to resistance against VEGF-monotherapy (PMID: 23103956). These pathways interact through receptor crosstalk and shared downstream signaling cascades, such as the MAPK/ERK and PI3K/Akt pathways, to enhance endothelial cell survival, proliferation, and migration (PMID: 15150101). Therapeutic strategies targeting this complex involve multi-kinase inhibitors like lenvatinib and nintedanib that block both VEGFR and FGFR (PMID: 24831325). This dual inhibition is designed to provide more comprehensive inhibition of the angiogenic process and overcome adaptive resistance in solid tumors. Beyond oncology, this signaling axis is also relevant in ophthalmology for treating neovascular diseases like age-related macular degeneration (PMID: 21829115). Clinical monitoring of this target often involves assessing circulating growth factor levels or vascular density in tumor tissues.

Other names

VEGF/FGF signaling crosstalkVEGFR-FGFR signaling axisbFGF-VEGF angiogenic complexVEGFR/FGFR dual targetFGF2-VEGF-A signaling complex

Simultaneous inhibition of the intracellular tyrosine kinase domains of vascular endothelial growth factor receptors (VEGFR) and fibroblast growth factor receptors (FGFR) to block downstream pro-angiogenic signaling pathways (PMID: 24831325).