Department of Sleep Medicine and Metabolic Disorders, Medical University of Lodz, 92-215 Lodz, Poland.
Department of Affective and Psychotic Disorders, Medical University of Lodz, 92-215 Lodz, Poland.
Int J Mol Sci. 2021 Nov 21;22(22):12536. doi: 10.3390/ijms222212536.
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.
阻塞性睡眠呼吸暂停（OSA）是一种慢性疾病，其特征是睡眠期间呼吸反复暂停，导致缺氧及其两个主要的病理后果：氧化应激和慢性炎症。这两者也与细胞衰老有关。由于 OSA 患者更容易出现与年龄相关的疾病，如心房高血压或 2 型糖尿病，因此可以观察到 OSA 与加速衰老之间存在关联。此外，已经确定这些 OSA 与端粒缩短有关。OSA 中的这个过程可能是由于活性氧（ROS）水平升高导致的氧化 DNA 损伤增加、DNA 修复中断、缺氧、慢性炎症和昼夜节律紊乱所致。本综述的目的是总结 OSA 患者白细胞端粒长度（LTL）变化的研究结果，并描述连接细胞衰老和 OSA 病理生理学的可能分子机制。由于氧化应激、缺氧和炎症，大多数 OSA 患者的 LTL 损耗特征明显，这形成了一种正反馈循环，并导致昼夜节律紊乱。
