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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Bibliographic Details
Published in:International journal of molecular sciences 2021-11, Vol.22 (22), p.12536
Main Authors: Turkiewicz, Szymon, Ditmer, Marta, Sochal, Marcin, Białasiewicz, Piotr, Strzelecki, Dominik, Gabryelska, Agata
Format: Article
Language:English
Subjects:
Age
Aging
Aging - genetics
Apnea
Biological clocks
Body mass index
Cell cycle
Cell division
Cellular Senescence - genetics
Cellular Senescence - physiology
Circadian rhythms
Complications
Deoxyribonucleic acid
Diabetes mellitus
Diabetes mellitus (non-insulin dependent)
DNA
DNA damage
DNA repair
Feedback loops
Humans
Hypertension
Hypoxia
Inflammation
Insomnia
Leukocytes - metabolism
Molecular modelling
OSA
Oxidative stress
Oxidative Stress - genetics
Positive feedback
Reactive oxygen species
Review
SASP
Senescence
Sleep apnea
Sleep Apnea, Obstructive - genetics
Sleep Apnea, Obstructive - pathology
Sleep disorders
Telomere - genetics
telomere shortening
Telomere Shortening - genetics
Telomeres
Womens health
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Summary: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.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms222212536