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Anti-VEGF receptor-2 monoclonal antibody prevents portal-systemic collateral vessel formation in portal hypertensive
Mercedes Fernandez1, Francesco Vizzutti, Juan Carlos Garcia-Pagan
1Hepatic Hemodynamic Laboratory, Liver Unit, Insitut d'Investigacions Biomediques August Pi i Sunyer, Hospital Clinic, Universityof Barcelona, Spain. mlobato@medicina.ub.es
Gastroenterology
|February 28, 2004
Summary
Portal hypertension leads to dangerous collateral vessels. Blocking vascular endothelial growth factor (VEGF) signaling inhibits this vessel formation, offering potential new therapies for liver disease patients.
Area of Science:
- Hepatology and Vascular Biology
- Investigating the molecular mechanisms of liver disease complications
Background:
- Portal hypertension is a common complication of chronic liver disease, leading to life-threatening gastroesophageal varices.
- The formation of portal-systemic collateral vessels is a key factor in the serious clinical outcomes of portal hypertension.
Purpose of the Study:
- To investigate the role of vascular endothelial growth factor (VEGF) in the development of portal-systemic collateral vessels.
- To determine if targeting VEGF signaling can inhibit collateral vessel formation in a murine model of portal hypertension.
Main Methods:
- Utilized a murine model of portal hypertension induced by partial portal vein ligation.
- Assessed the impact of anti-VEGF receptor-2 monoclonal antibodies and a specific VEGF receptor-2 autophosphorylation inhibitor on collateral vessel formation.
Main Results:
- Treatment with anti-VEGF receptor-2 antibodies significantly inhibited collateral vessel formation in mice.
- Inhibition of VEGF receptor-2 autophosphorylation markedly reduced collateral vessel formation in rats.
Conclusions:
- Collateral vessel formation in portal hypertension is an angiogenesis-dependent process.
- Blocking the VEGF signaling pathway effectively inhibits the development of these critical vessels.
- These findings highlight angiogenesis as a therapeutic target for portal hypertension.
