Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening

Obstructive sleep apnea (OSA) is chronic disorder which is characterized by recurrent pauses of breathing during sleep which leads to hypoxia and its two main pathological sequelae: oxidative stress and chronic inflammation. Both are also associated with cellular senescence. As OSA patients present...

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Autores principales: Szymon Turkiewicz, Marta Ditmer, Marcin Sochal, Piotr Białasiewicz, Dominik Strzelecki, Agata Gabryelska
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Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/96d669c2fe684c0dad823c0fbfb73cd0
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spelling oai:doaj.org-article:96d669c2fe684c0dad823c0fbfb73cd02021-11-25T17:57:35ZObstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening10.3390/ijms2222125361422-00671661-6596https://doaj.org/article/96d669c2fe684c0dad823c0fbfb73cd02021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/22/12536https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Obstructive sleep apnea (OSA) is chronic disorder which is characterized by recurrent pauses of breathing during sleep which leads to hypoxia and its two main pathological sequelae: oxidative stress and chronic inflammation. Both are also associated with cellular senescence. As OSA patients present with higher prevalence of age-related disorders, such as atrial hypertension or diabetes mellitus type 2, a relationship between OSA and accelerated aging is observable. Furthermore, it has been established that these OSA are associated with telomere shortening. This process in OSA is likely caused by increased oxidative DNA damage due to increased reactive oxygen species levels, DNA repair disruptions, hypoxia, chronic inflammation, and circadian clock disturbances. The aim of the review is to summarize study outcomes on changes in leukocyte telomere length (LTL) in OSA patients and describe possible molecular mechanisms which connect cellular senescence and the pathophysiology of OSA. The majority of OSA patients are characterized by LTL attrition due to oxidative stress, hypoxia and inflammation, which make a kind of positive feedback loop, and circadian clock disturbance.Szymon TurkiewiczMarta DitmerMarcin SochalPiotr BiałasiewiczDominik StrzeleckiAgata GabryelskaMDPI AGarticleOSAsenescencetelomere shorteningSASPhypoxiainflammationBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12536, p 12536 (2021)
institution DOAJ
collection DOAJ
language EN
topic OSA
senescence
telomere shortening
SASP
hypoxia
inflammation
Biology (General)
QH301-705.5
Chemistry
QD1-999
spellingShingle OSA
senescence
telomere shortening
SASP
hypoxia
inflammation
Biology (General)
QH301-705.5
Chemistry
QD1-999
Szymon Turkiewicz
Marta Ditmer
Marcin Sochal
Piotr Białasiewicz
Dominik Strzelecki
Agata Gabryelska
Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening
description Obstructive sleep apnea (OSA) is chronic disorder which is characterized by recurrent pauses of breathing during sleep which leads to hypoxia and its two main pathological sequelae: oxidative stress and chronic inflammation. Both are also associated with cellular senescence. As OSA patients present with higher prevalence of age-related disorders, such as atrial hypertension or diabetes mellitus type 2, a relationship between OSA and accelerated aging is observable. Furthermore, it has been established that these OSA are associated with telomere shortening. This process in OSA is likely caused by increased oxidative DNA damage due to increased reactive oxygen species levels, DNA repair disruptions, hypoxia, chronic inflammation, and circadian clock disturbances. The aim of the review is to summarize study outcomes on changes in leukocyte telomere length (LTL) in OSA patients and describe possible molecular mechanisms which connect cellular senescence and the pathophysiology of OSA. The majority of OSA patients are characterized by LTL attrition due to oxidative stress, hypoxia and inflammation, which make a kind of positive feedback loop, and circadian clock disturbance.
format article
author Szymon Turkiewicz
Marta Ditmer
Marcin Sochal
Piotr Białasiewicz
Dominik Strzelecki
Agata Gabryelska
author_facet Szymon Turkiewicz
Marta Ditmer
Marcin Sochal
Piotr Białasiewicz
Dominik Strzelecki
Agata Gabryelska
author_sort Szymon Turkiewicz
title Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening
title_short Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening
title_full Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening
title_fullStr Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening
title_full_unstemmed Obstructive Sleep Apnea as an Acceleration Trigger of Cellular Senescence Processes through Telomere Shortening
title_sort obstructive sleep apnea as an acceleration trigger of cellular senescence processes through telomere shortening
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/96d669c2fe684c0dad823c0fbfb73cd0
work_keys_str_mv AT szymonturkiewicz obstructivesleepapneaasanaccelerationtriggerofcellularsenescenceprocessesthroughtelomereshortening
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AT piotrbiałasiewicz obstructivesleepapneaasanaccelerationtriggerofcellularsenescenceprocessesthroughtelomereshortening
AT dominikstrzelecki obstructivesleepapneaasanaccelerationtriggerofcellularsenescenceprocessesthroughtelomereshortening
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