Vascular endothelial growth factor (VEGF) in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS): paradox or paradigm?
- 1 July 2006
- Vol. 61 (7) , 621-626
- https://doi.org/10.1136/thx.2005.040204
Abstract
Acute respiratory distress syndrome (ARDS), the most severe form of acute lung injury (ALI), remains a devastating condition with a high mortality. It is characterised by alveolar injury and increased pulmonary vascular permeability. Vascular endothelial cell growth factor (VEGF) was identified by its properties to increase permeability and act as a cellular growth factor, hence its potential for a key role in the pathogenesis of ALI/ARDS. This review describes the basic biology of VEGF and its receptors as an essential prerequisite to discussing the available and sometimes paradoxical published data, before considering a paradigm for the role of VEGF in the human lung.Keywords
This publication has 100 references indexed in Scilit:
- Regulation of vascular endothelial growth factor bioactivity in patients with acute lung injuryThorax, 2005
- The biology of VEGF and its receptorsNature Medicine, 2003
- Vascular endothelial growth factor mRNA and protein expression in airway epithelial cell linesin vitroEuropean Respiratory Journal, 2002
- VEGF165 mediates formation of complexes containing VEGFR‐2 and neuropilin‐1 that enhance VEGF165‐receptor bindingJournal of Cellular Biochemistry, 2002
- The Acute Respiratory Distress SyndromeNew England Journal of Medicine, 2000
- Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress SyndromeNew England Journal of Medicine, 2000
- Abnormal blood vessel development and lethality in embryos lacking a single VEGF alleleNature, 1996
- Role of the Flt-1 receptor tyrosine kinase in regulating the assembly of vascular endotheliumNature, 1995
- Failure of blood-island formation and vasculogenesis in Flk-1-deficient miceNature, 1995
- Inhibition of vascular endothelial cell growth factor activity by an endogenously encoded soluble receptor.Proceedings of the National Academy of Sciences, 1993