Abstract
There 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-κB 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.
SERIES “THE GENETIC AND CARDIOVASCULAR ASPECTS OF OBSTRUCTIVE SLEEP APNOEA/HYPOPNOEA SYNDROME”
Edited by R.L. Riha and W.T. McNicholas
Number 4 in this Series
Footnotes
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Previous articles in this series: No. 1: MacLeod AK, Liewald DCM, McGilchrist MM, Morris AD, Kerr SM, Porteous DJ. Some principles and practices of genetic biobanking studies. Eur Respir J 2009; 33: 419–425. No. 2: Riha RL, Gislasson T, Diefenbach K. The phenotype and genotype of adult obstructive sleep apnoea/hypopnoea syndrome. Eur Respir J 2009; 33: 646–655. No. 3: Jennum P, Riha RL. Epidemiology of sleep apnoea/hypopnoea syndrome and sleep-disordered breathing. Eur Respir J 2009; 33: 907–914.
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