Clinical implications for vascular endothelial growth factor in the lung: friend or foe?
Vascular endothelial growth factor (VEGF) is a potent mediator of angiogenesis which has multiple effects in lung development and physiology. VEGF is expressed in several parts of the lung and the pleura while it has been shown that changes in its expression play a significant role in the pathophysiology of some of the most common respiratory disorders, such as acute lung injury, asthma, chronic obstructive pulmonary disease, obstructive sleep apnea, idiopathic pulmonary fibrosis, pulmonary hypertension, pleural disease, and lung cancer. However, the exact role of VEGF in the lung is not clear yet, as there is contradictory evidence that suggests either a protective or a harmful role. VEGF seems to interfere in a different manner, depending on its amount, the location, and the underlying pathologic process in lung tissue. The lack of VEGF in some disease entities may provide implications for its substitution, whereas its overexpression in other lung disorders has led to interventions for the attenuation of its action. Many efforts have been made in order to regulate the expression of VEGF and anti-VEGF antibodies are already in use for the management of lung cancer. Further research is still needed for the complete understanding of the exact role of VEGF in health and disease, in order to take advantage of its benefits and avoid its adverse effects. The scope of the present review is to summarize from a clinical point of view the changes in VEGF expression in several disorders of the respiratory system and focus on its diagnostic and therapeutic implications.
Papaioannou
Andriana I
AI
Respiratory Medicine Department, University of Thessaly School of Medicine, University Hospital of Larissa, Larissa 41110, Greece. andriana78@panafonet.gr
Kostikas
Konstantinos
K
Kollia
Panagoula
P
Gourgoulianis
Konstantinos I
KI
D020533:Angiogenesis Inhibitors / Q000627:therapeutic use; D042682:Angiopoietins / Q000378:metabolism; D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D000068258:Bevacizumab; D036342:Ephrins / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000378:metabolism; D007211:Indoles / Q000494:pharmacology / Q000627:therapeutic use; D008168:Lung / Q000378:metabolism*; D008171:Lung Diseases / Q000188:drug therapy / Q000378:metabolism*; D010995:Pleural Diseases / Q000378:metabolism; D047428:Protein Kinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D011499:Protein Processing, Post-Translational; D011758:Pyrroles / Q000494:pharmacology / Q000627:therapeutic use; D040262:Receptors, Vascular Endothelial Growth Factor / Q000037:antagonists & inhibitors / Q000378:metabolism; D014158:Transcription, Genetic; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000276:immunology / Q000378:metabolism*
D020533:Angiogenesis Inhibitors; D042682:Angiopoietins; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D036342:Ephrins; D007211:Indoles; D047428:Protein Kinase Inhibitors; D011758:Pyrroles; D042461:Vascular Endothelial Growth Factor A; D000068258:Bevacizumab; C116890:Semaxinib; D040262:Receptors, Vascular Endothelial Growth Factor