angiogenesis
Definition
Angiogenesis is the physiological process of forming new blood vessels from pre-existing vasculature. This complex mechanism involves endothelial cell activation, proliferation, migration, and tube formation in response to pro-angiogenic signals like VEGF (vascular endothelial growth factor). Angiogenesis is essential for normal development, wound healing, and tissue regeneration, but becomes pathological in cancer, where tumors hijack this process to establish blood supply for growth and metastasis. The process is tightly regulated by a balance between pro-angiogenic factors (VEGF, FGF, PDGF) and anti-angiogenic factors (thrombospondin, endostatin). Understanding angiogenic pathways is critical for developing cancer therapeutics, treating ischemic diseases, and promoting tissue repair.
Visualize angiogenesis in Nodes Bio
Researchers can map angiogenic signaling networks by visualizing interactions between growth factors, receptors, and downstream effectors. Nodes Bio enables analysis of how VEGF pathway components connect to hypoxia-inducible factors, matrix metalloproteinases, and endothelial cell responses. Users can overlay gene expression data to identify key regulatory nodes and explore how anti-angiogenic drugs disrupt specific pathway connections in different tumor contexts.
Visualization Ideas:
- VEGF-centered signaling cascade showing receptor tyrosine kinase activation and downstream PI3K/AKT and MAPK pathways
- Multi-factor angiogenic network integrating VEGF, FGF, PDGF, and angiopoietin pathways with endothelial cell response genes
- Drug-target network mapping anti-angiogenic therapeutics to their molecular targets and affected downstream processes
Example Use Case
An oncology research team investigating resistance to bevacizumab (anti-VEGF therapy) in colorectal cancer uses network analysis to map alternative angiogenic pathways. By integrating RNA-seq data from resistant tumors, they visualize upregulation of FGF2 and angiopoietin signaling networks that bypass VEGF blockade. The network reveals that resistant tumors activate compensatory pathways through AKT and MAPK signaling, suggesting combination therapy targets. This analysis identifies FGFR inhibitors as potential partners to overcome resistance mechanisms.