ArticleiScience2025
A mechanistic computational model of HGF-VEGF-mediated endothelial cell proliferation and vascular permeability.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
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 require VEGFR2 activation to affect permeability and proliferation. This model has the potential to be applicable and helpful in analyzing angiogenesis-dependent diseases. It provided insights into the mechanisms of EC proliferation and vascular permeability induced by HGF and VEGF and permitted evaluation of their separate or combined effects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.