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Mechanisms of endothelial dysfunction in obstructive sleep apnea
Endothelial activation and inflammation are important mediators of accelerated atherogenesis and consequent increased cardiovascular morbidity in obstructive sleep apnea (OSA). Repetitive episodes of hypoxia/reoxygenation associated with transient cessation of breathing during sleep in OSA resemble...
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Formato: | Texto |
Lenguaje: | English |
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Dove Medical Press
2008
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2663447/ https://www.ncbi.nlm.nih.gov/pubmed/19337546 |
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author | Atkeson, Amy Jelic, Sanja |
author_facet | Atkeson, Amy Jelic, Sanja |
author_sort | Atkeson, Amy |
collection | PubMed |
description | Endothelial activation and inflammation are important mediators of accelerated atherogenesis and consequent increased cardiovascular morbidity in obstructive sleep apnea (OSA). Repetitive episodes of hypoxia/reoxygenation associated with transient cessation of breathing during sleep in OSA resemble ischemia/reperfusion injury and may be the main culprit underlying endothelial dysfunction in OSA. Additional factors such as repetitive arousals resulting in sleep fragmentation and deprivation and individual genetic suseptibility to vascular manifestations of OSA contribute to impaired endothelial function in OSA. The present review focuses on possible mechanisms that underlie endothelial activation and inflammation in OSA. |
format | Text |
id | pubmed-2663447 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-26634472009-04-01 Mechanisms of endothelial dysfunction in obstructive sleep apnea Atkeson, Amy Jelic, Sanja Vasc Health Risk Manag Review Endothelial activation and inflammation are important mediators of accelerated atherogenesis and consequent increased cardiovascular morbidity in obstructive sleep apnea (OSA). Repetitive episodes of hypoxia/reoxygenation associated with transient cessation of breathing during sleep in OSA resemble ischemia/reperfusion injury and may be the main culprit underlying endothelial dysfunction in OSA. Additional factors such as repetitive arousals resulting in sleep fragmentation and deprivation and individual genetic suseptibility to vascular manifestations of OSA contribute to impaired endothelial function in OSA. The present review focuses on possible mechanisms that underlie endothelial activation and inflammation in OSA. Dove Medical Press 2008-12 /pmc/articles/PMC2663447/ /pubmed/19337546 Text en © 2008 Atkeson and Jelic, publisher and licensee Dove Medical Press Ltd. This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited. |
spellingShingle | Review Atkeson, Amy Jelic, Sanja Mechanisms of endothelial dysfunction in obstructive sleep apnea |
title | Mechanisms of endothelial dysfunction in obstructive sleep apnea |
title_full | Mechanisms of endothelial dysfunction in obstructive sleep apnea |
title_fullStr | Mechanisms of endothelial dysfunction in obstructive sleep apnea |
title_full_unstemmed | Mechanisms of endothelial dysfunction in obstructive sleep apnea |
title_short | Mechanisms of endothelial dysfunction in obstructive sleep apnea |
title_sort | mechanisms of endothelial dysfunction in obstructive sleep apnea |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2663447/ https://www.ncbi.nlm.nih.gov/pubmed/19337546 |
work_keys_str_mv | AT atkesonamy mechanismsofendothelialdysfunctioninobstructivesleepapnea AT jelicsanja mechanismsofendothelialdysfunctioninobstructivesleepapnea |