Basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF), and their receptors (FGFR and VEGFR) (bFGF/VEGF/FGFR/VEGFR)

The basic Fibroblast Growth Factor (bFGF/FGF2) and Vascular Endothelial Growth Factor (VEGF) pathways, including their respective receptors (FGFR and VEGFR), are fundamental regulators of angiogenesis and vascular homeostasis (Ferrara, 2004; Presta et al., 2005). VEGF is a primary mediator of endothelial cell proliferation and vascular permeability, while bFGF acts as a potent mitogen for a wide range of cells, often synergizing with VEGF to drive pathological neovascularization (UniProt P09038; UniProt P15692). In oncology, these pathways are frequently co-opted by tumors to establish a blood supply, which is essential for sustained growth and metastatic spread (Hanahan & Weinberg, 2011). Therapeutic strategies targeting these molecules include monoclonal antibodies that neutralize the ligands and small-molecule tyrosine kinase inhibitors (TKIs) that block receptor signaling (StatPearls, 2023). Multi-kinase inhibitors like nintedanib and lenvatinib are specifically designed to hit both FGFR and VEGFR families to overcome resistance mechanisms (DrugBank, 2024). While effective in treating various cancers and neovascular eye diseases, these therapies often lead to class-specific toxicities such as hypertension, proteinuria, and wound healing complications due to the disruption of physiological vascular maintenance (FDA, 2024). Understanding the interplay between these two growth factor systems is crucial for optimizing anti-angiogenic therapy and managing potential resistance (PubMed, 2023).

Other names

bFGFVEGFFGF2VEGFAFGFRVEGFRFibroblast growth factor 2Vascular endothelial growth factor AHeparin-binding growth factor 2Vascular permeability factor

Inhibition of ligand-receptor interaction (e.g., monoclonal antibodies or decoy receptors) or inhibition of the intracellular tyrosine kinase domain (e.g., small-molecule TKIs), thereby blocking downstream signaling cascades like MAPK/ERK, PI3K/Akt, and PLCγ that drive angiogenesis and cell survival (StatPearls, 2023; Presta et al., 2005).