A mechanistic computational model of HGF-VEGF-mediated endothelial cell proliferation and vascular permeability.

ABSTRACT: Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are important pro-angiogenic factors in angiogenesis-dependent diseases. While sharing some signaling pathways, their contrasting effect on vascular permeability remains under investigation. To explore how these factors promote angiogenesis, we developed, calibrated, and validated a data-driven mechanistic computational model of HGF and VEGF signaling in endothelial cells (ECs). We proposed that variations in permeability profiles may stem from RAC1-PAK1 activation via site-specific phosphorylation. By introducing permeability and proliferation indices, our simulations indicated a dose-dependent effect of VEGF that hampered the ability of HGF to promote vascular stability. Our simulations indicate that HGF did not

SUBMITTER: de Melo Oliveira RH 

PROVIDER: S-EPMC12355113 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature