Obstructive Sleep Apnea and Hallmarks of Aging

Obstructive sleep apnea (OSA) prevalence has substantially increased over the past two decades and, in industrialized countries, it is estimated to become one of the most common chronic diseases. OSA has recently been associated with earlier cognitive decline; thus, OSA treatment might delay aging-associated functional decline. OSA-associated epigenetic changes may underlie disease-associated heterogeneity in terms of symptoms, outcomes, and even treatment response. Telomere length is reduced in leukocytes from patients with OSA, suggesting accelerated cellular aging and inducing a higher risk for age-related diseases. Blood-circulating endothelial progenitor cells may be reduced in patients with OSA, compromising the endothelial repair capacity and contributing to endothelial apoptosis. Obstructive sleep apnea (OSA) is one of the most common sleep disorders. Since aging is a risk factor for OSA development, it is expected that its prevalence will increase with the current increase in life span. In recent years, several studies have shown that OSA potentially contributes to functional decline, mainly prompted by chronic intermittent hypoxia and sleep fragmentation. Here, we propose that OSA might anticipate/aggravate aging by inducing cellular and molecular impairments that characterize the aging process, such as stem cell exhaustion, telomere attrition and epigenetic changes. We suggest that further knowledge on the impact of OSA on aging mechanisms might contribute to a better understanding of how OSA might putatively accelerate aging and aging-related diseases. Obstructive sleep apnea (OSA) is one of the most common sleep disorders. Since aging is a risk factor for OSA development, it is expected that its prevalence will increase with the current increase in life span. In recent years, several studies have shown that OSA potentially contributes to functional decline, mainly prompted by chronic intermittent hypoxia and sleep fragmentation. Here, we propose that OSA might anticipate/aggravate aging by inducing cellular and molecular impairments that characterize the aging process, such as stem cell exhaustion, telomere attrition and epigenetic changes. We suggest that further knowledge on the impact of OSA on aging mechanisms might contribute to a better understanding of how OSA might putatively accelerate aging and aging-related diseases. a surgical operation to remove both the adenoids and tonsils. the endogenously regulated cellular ‘housekeeping’ mechanism responsible for the degradation of damaged and dysfunctional cellular organelles and protein aggregates. assesses three categories related to the risk of suffering OSA: (i) presence and frequency of snoring behavior; (ii) wake-time sleepiness or fatigue; and (iii) history of obesity and/or hypertension. Patients can be classified as high risk or low risk based on their responses to individual items and their overall scores in symptom categories. small, extranuclear bodies that arise in dividing cells from fragmented chromosomes (without centromere) or whole chromosomes and/or chromatids lagging behind in anaphase. the stable arrest of the cell cycle attributable to stereotyped phenotypic changes. a device connected to a nasal or facial mask that supports breathing during sleep. CPAP blows compressed air into the airways and keeps the upper airway free. circulating cells that express a variety of cell surface markers similar to those expressed by vascular endothelial cells, adhere to endothelium at sites of hypoxia and/or ischemia, and participate in new vessel formation. measures daytime sleepiness. It comprises a questionnaire that assesses retrospective reports of the likelihood of dozing off or falling asleep in different situations. The total score estimates whether the individual experiences daytime sleepiness that requires medical attention. cell-derived vesicles, present in biological fluids, involved in intercellular communication (via transfer of proteins, lipids and nucleic acids) and regulation of normal physiological processes. the ability of glucose to facilitate its own disposal independent of an insulin response. a central component of the cellular network of molecular chaperones and folding catalysts. repeated episodes of hypoxia (any oxygen levels lower than normoxia) interspersed with normoxia (earth atmosphere oxygen level ≈21% O2) or less hypoxic conditions. adult, nonhematopoietic, multipotent stem cells with the capacity to differentiate into mesodermal lineages, such as osteocytes, adipocytes, and chondrocytes, as well ectodermal (neurocytes) and endodermal lineages (hepatocytes). originate from dicentric chromosomes, which may occur due to misrepair of DNA breaks, telomere end fusions, or the defective separation of sister chromatids at anaphase. nuclear anomalies associated with chromosomal instability events, commonly seen in cancer. an overnight sleep test, performed in-laboratory, able to monitor sleep time and stages (electroencephalogram; EEG), eye movements (electrooculogram), muscle tone (chin electromyogram), heart rhythm (electrocardiogram), airflow, thoracic and abdominal respiratory effort, arterial oxygen saturation (oximetry) and carbon dioxide levels (capnography), body orientation, limb movements (leg electromyogram), and snoring. used to assess endothelial function, based on blood perfusion measurements before, during, and after occlusion. the ability of the proteasome to degrade unneeded or damaged proteins by proteolysis. involves mechanisms for the stabilization of correctly folded proteins, most prominently, the heatshock family of proteins, and mechanisms for the degradation of proteins (i.e., proteasome, lysosome, or autophagy-mediated mechanisms). results from protein misfolding or aggregation, which may impair cellular function and may affect the fate of nonrenewable cells of long-lived organisms. a senescent cellular state characterized by an increased release of inflammatory cytokines and chemokines. brief awakenings or microarousals during the sleep period that induce short increases in EEG frequency. Such episodes may occur spontaneously or in response to respiratory events or tones. decrease in the number and functional competence of adult stem cells, compromising their role in tissue renewal. one of the most validated screening and predictive tools developed to estimate the probability of OSA in various clinical populations. It assesses snoring, fatigue, observed events, blood pressure, BMI, age, neck circumference, and gender. the progressive and cumulative loss of telomere-protective sequences from chromosome ends that explains the limited proliferative capacity of some types of cell. recognize specific patterns of microbial components, especially those from pathogens, and regulate the activation of both innate and adaptive immunity. an adaptive response to endoplasmic reticulum (ER) stress, restoring ER homeostasis. a population of epiblast-derived cells that express several markers of pluripotent stem cells (PSC) that are characteristic for epiblast/germ line-derived stem cells. VSELs are deposited during early gastrulation in developing tissues and/or organs and have an important role in the turnover of tissue-specific and/or committed stem cells.