Pleural effusion is a common clinical problem in everyday clinical practice. Vascular endothelial growth factor (VEGF) is a 34-45 kDa homodimeric glycoprotein, which is a potent mediator of angiogenesis and vascular permeability. VEGF is present in significant quantities in pleural effusions of different origins, and its levels are consistently higher in exudates than in transudates. There is compelling experimental evidence demonstrating that VEGF is a crucial mediator in fluid formation. In the pleural space mesothelial cells are likely the principal source of fluid VEGF. It is also produced by most malignant cell types and inflammatory cells including lymphocytes, eosinophils, macrophages, and neutrophls. VEGF production can be stimulated by various cytokines, among which transforming growth factor beta (TGF-β) appears to be the most potent and consistent. Hypoxia and ischemia are the most established physical stimulators of VEGF. Promising results are rapidly accumulating on the use of VEGF inhibition in preventing pleural fluid accumulation; clinical trials are underway using VEGF antagonists in the management of malignant pleural effusions. The main focus of this review is to evaluate the role of VEGF in the pathogenesis and differential diagnosis of pleural effusions as well as the therapeutic implications of VEGF in control of effusions formation.
Keywords: Angiogenesis, pleural effusion, vascular endothelial growth factor, transforming growth factor, tyrosine-kinase receptors, hypoxia, empyema, Staphylococcus aureus, tuberculosis
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