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- Publisher Website: 10.2174/138920008785821684
- Scopus: eid_2-s2.0-52449133912
- PMID: 18781916
- WOS: WOS:000259447600008
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Article: Dysfunction of pulmonary vascular endothelium in chronic obstructive pulmonary disease: Basic considerations for future drug development
Title | Dysfunction of pulmonary vascular endothelium in chronic obstructive pulmonary disease: Basic considerations for future drug development |
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Authors | |
Keywords | Adhesion molecules Chronic obstructive pulmonary disease Endothelium-derived relaxing factors Pulmonary endothelium Vascular progenitor cells VEGF |
Issue Date | 2008 |
Citation | Current Drug Metabolism, 2008, v. 9 n. 7, p. 661-667 How to Cite? |
Abstract | Chronic obstructive pulmonary disease (COPD) is one of the leading health problems worldwide and continues to be a major cause of morbidity and mortality in developed countries. The clinical features of COPD are chronic obstructive bronchiolitis and emphysema. Pulmonary vascular endothelial dysfunction is a characteristic pathological finding of COPD at different stages of the disease. Functional changes of pulmonary endothelial cells in COPD include antiplatelet abnormalities, anticoagulant disturbances, endothelial activation, atherogenesis, and compromised regulation of vascular tone which may adversely affect the ventilation-perfusion match in COPD. As the most important risk factor of COPD, cigarette smoking may initiate pulmonary vascular impairment through direct injury of endothelial cells or release of inflammatory mediators. Morphological changes such as denudation of endothelium and endothelial cell apoptosis have been observed in the pulmonary vasculature in COPD patients as well as functional alterations. Changes in the expression of tissue factor pathway inhibitor (TFPI), thrombomodulin, selectins, and adhesion molecules in pulmonary endothelial cells as well as complex regulation and interaction of vasoactive substances and growth factors released from endothelium may underlie the mechanisms of pulmonary endothelial dysfunction in COPD. The mechanism of endothelial repair/regeneration in COPD, although not fully understood, may involve upregulation of vascular endothelial growth factors in the early stages along with an increased number of bone marrow-derived progenitor cells. These factors should be taken into account when developing new strategies for the pharmacological therapy of patients with COPD. © 2008 Bentham Science Publishers Ltd. |
Persistent Identifier | http://hdl.handle.net/10722/192667 |
ISSN | 2023 Impact Factor: 2.1 2023 SCImago Journal Rankings: 0.453 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Yang, Q | en_US |
dc.contributor.author | Underwood, MJ | en_US |
dc.contributor.author | Hsin, MKY | en_US |
dc.contributor.author | Liu, X-C | en_US |
dc.contributor.author | He, G-W | en_US |
dc.date.accessioned | 2013-11-20T04:55:01Z | - |
dc.date.available | 2013-11-20T04:55:01Z | - |
dc.date.issued | 2008 | en_US |
dc.identifier.citation | Current Drug Metabolism, 2008, v. 9 n. 7, p. 661-667 | en_US |
dc.identifier.issn | 1389-2002 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/192667 | - |
dc.description.abstract | Chronic obstructive pulmonary disease (COPD) is one of the leading health problems worldwide and continues to be a major cause of morbidity and mortality in developed countries. The clinical features of COPD are chronic obstructive bronchiolitis and emphysema. Pulmonary vascular endothelial dysfunction is a characteristic pathological finding of COPD at different stages of the disease. Functional changes of pulmonary endothelial cells in COPD include antiplatelet abnormalities, anticoagulant disturbances, endothelial activation, atherogenesis, and compromised regulation of vascular tone which may adversely affect the ventilation-perfusion match in COPD. As the most important risk factor of COPD, cigarette smoking may initiate pulmonary vascular impairment through direct injury of endothelial cells or release of inflammatory mediators. Morphological changes such as denudation of endothelium and endothelial cell apoptosis have been observed in the pulmonary vasculature in COPD patients as well as functional alterations. Changes in the expression of tissue factor pathway inhibitor (TFPI), thrombomodulin, selectins, and adhesion molecules in pulmonary endothelial cells as well as complex regulation and interaction of vasoactive substances and growth factors released from endothelium may underlie the mechanisms of pulmonary endothelial dysfunction in COPD. The mechanism of endothelial repair/regeneration in COPD, although not fully understood, may involve upregulation of vascular endothelial growth factors in the early stages along with an increased number of bone marrow-derived progenitor cells. These factors should be taken into account when developing new strategies for the pharmacological therapy of patients with COPD. © 2008 Bentham Science Publishers Ltd. | en_US |
dc.language | eng | en_US |
dc.relation.ispartof | Current Drug Metabolism | en_US |
dc.subject | Adhesion molecules | - |
dc.subject | Chronic obstructive pulmonary disease | - |
dc.subject | Endothelium-derived relaxing factors | - |
dc.subject | Pulmonary endothelium | - |
dc.subject | Vascular progenitor cells | - |
dc.subject | VEGF | - |
dc.title | Dysfunction of pulmonary vascular endothelium in chronic obstructive pulmonary disease: Basic considerations for future drug development | en_US |
dc.type | Article | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.2174/138920008785821684 | en_US |
dc.identifier.pmid | 18781916 | - |
dc.identifier.scopus | eid_2-s2.0-52449133912 | en_US |
dc.identifier.volume | 9 | en_US |
dc.identifier.issue | 7 | en_US |
dc.identifier.spage | 661 | en_US |
dc.identifier.epage | 667 | en_US |
dc.identifier.isi | WOS:000259447600008 | - |
dc.identifier.issnl | 1389-2002 | - |