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dc.contributor.authorGarvey, J F
dc.contributor.authorTaylor, C T
dc.contributor.authorMcNicholas, W T
dc.date.accessioned2012-02-01T10:34:19Z
dc.date.available2012-02-01T10:34:19Z
dc.date.issued2012-02-01T10:34:19Z
dc.identifier.citationEur Respir J. 2009 May;33(5):1195-205.en_GB
dc.identifier.issn1399-3003 (Electronic)en_GB
dc.identifier.issn0903-1936 (Linking)en_GB
dc.identifier.pmid19407053en_GB
dc.identifier.doi10.1183/09031936.00111208en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207663
dc.description.abstractThere is increasing evidence that intermittent hypoxia plays a role in the development of cardiovascular risk in obstructive sleep apnoea syndrome (OSAS) through the activation of inflammatory pathways. The development of translational models of intermittent hypoxia has allowed investigation of its role in the activation of inflammatory mechanisms and promotion of cardiovascular disease in OSAS. There are noticeable differences in the response to intermittent hypoxia between body tissues but the hypoxia-sensitive transcription factors hypoxia-inducible factor-1 and nuclear factor-kappaB appear to play a key role in mediating the inflammatory and cardiovascular consequences of OSAS. Expanding our understanding of these pathways, the cross-talk between them and the activation of inflammatory mechanisms by intermittent hypoxia in OSAS will provide new avenues of therapeutic opportunity for the disease.
dc.language.isoengen_GB
dc.subject.meshAnimalsen_GB
dc.subject.meshAnoxia/physiopathologyen_GB
dc.subject.meshCardiovascular Diseases/*physiopathologyen_GB
dc.subject.meshCytokines/physiologyen_GB
dc.subject.meshHumansen_GB
dc.subject.meshInflammation/physiopathologyen_GB
dc.subject.meshSleep Apnea, Obstructive/*physiopathologyen_GB
dc.subject.meshTranscription Factors/physiologyen_GB
dc.titleCardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation.en_GB
dc.contributor.departmentRespiratory Sleep Disorders Unit, St. Vincent's University Hospital, Dublin,, Ireland.en_GB
dc.identifier.journalThe European respiratory journal : official journal of the European Society for, Clinical Respiratory Physiologyen_GB
dc.description.provinceLeinster
html.description.abstractThere is increasing evidence that intermittent hypoxia plays a role in the development of cardiovascular risk in obstructive sleep apnoea syndrome (OSAS) through the activation of inflammatory pathways. The development of translational models of intermittent hypoxia has allowed investigation of its role in the activation of inflammatory mechanisms and promotion of cardiovascular disease in OSAS. There are noticeable differences in the response to intermittent hypoxia between body tissues but the hypoxia-sensitive transcription factors hypoxia-inducible factor-1 and nuclear factor-kappaB appear to play a key role in mediating the inflammatory and cardiovascular consequences of OSAS. Expanding our understanding of these pathways, the cross-talk between them and the activation of inflammatory mechanisms by intermittent hypoxia in OSAS will provide new avenues of therapeutic opportunity for the disease.


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