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Article: Dysfunction of pulmonary vascular endothelium in chronic obstructive pulmonary disease: Basic considerations for future drug development

TitleDysfunction of pulmonary vascular endothelium in chronic obstructive pulmonary disease: Basic considerations for future drug development
Authors
Issue Date2008
Citation
Current Drug Metabolism, 2008, v. 9 n. 7, p. 661-667 How to Cite?
AbstractChronic 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 Identifierhttp://hdl.handle.net/10722/192667
ISSN
2015 Impact Factor: 2.847
2015 SCImago Journal Rankings: 0.976
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYang, Qen_US
dc.contributor.authorUnderwood, MJen_US
dc.contributor.authorHsin, MKYen_US
dc.contributor.authorLiu, X-Cen_US
dc.contributor.authorHe, G-Wen_US
dc.date.accessioned2013-11-20T04:55:01Z-
dc.date.available2013-11-20T04:55:01Z-
dc.date.issued2008en_US
dc.identifier.citationCurrent Drug Metabolism, 2008, v. 9 n. 7, p. 661-667en_US
dc.identifier.issn1389-2002en_US
dc.identifier.urihttp://hdl.handle.net/10722/192667-
dc.description.abstractChronic 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.languageengen_US
dc.relation.ispartofCurrent Drug Metabolismen_US
dc.titleDysfunction of pulmonary vascular endothelium in chronic obstructive pulmonary disease: Basic considerations for future drug developmenten_US
dc.typeArticleen_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.2174/138920008785821684en_US
dc.identifier.pmid18781916-
dc.identifier.scopuseid_2-s2.0-52449133912en_US
dc.identifier.volume9en_US
dc.identifier.issue7en_US
dc.identifier.spage661en_US
dc.identifier.epage667en_US
dc.identifier.isiWOS:000259447600008-

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