Correlation between insomnia and telomere length and aging
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摘要: 睡眠是由大脑中的睡眠促进和唤醒中心调控的一种神经化学过程。随着年龄的增长,昼夜节律的稳定性降低,睡眠障碍的患病率增加。失眠是最常见的睡眠障碍,影响着数以百万计的人,对个人和社会都有着深远的影响。与青壮年相比,老年人的睡眠模式、睡眠时间和质量都发生了显著的变化,如睡眠片段化、早醒、慢波睡眠减少等,失眠的发生率明显升高。长期严重的失眠不仅给患者的生活质量造成影响,甚至与某些疾病的发病风险、死亡率增加有关。目前与年龄相关的睡眠模式改变的机制尚不完全清楚。然而,这并不意味着失眠是衰老的正常现象。端粒是真核生物染色体的末端,在转录过程中,其对染色体末端保护和基因组稳定性维护发挥着重要作用,同时在控制细胞衰老和机体衰老中起着核心作用。端粒长度的缩短或端粒结构的改变,最终会导致细胞的复制性衰老和染色体的不稳定性, 这两者都是衰老的标志。衰老是生命的必然结果,在大多数生物体中,衰老的速度与平均寿命成反比。年龄增长也是癌症、神经退行性变和心血管疾病的最大危险因素。目前有关于失眠与端粒长度、衰老之间关系的两两研究,然而缺乏对三者之间的系统综述,本文将从失眠对端粒长度的影响、端粒长度对衰老的意义以及失眠对衰老的影响3个方面进行阐述。Abstract: Sleep is a neurochemical process regulated by sleep promotion and arousal centres in the brain. Circadian rhythm stability decreases with age, and the prevalence of sleep disorders increases. Insomnia is the most common sleep disorder, and it affects millions of people and has profound consequences for individuals and society. The sleep pattern, sleep duration and quality of elderly have undergone significant changes, such as sleep fragmentation, early awakening, slow wave sleep reduction and significantly increased incidence of insomnia, compared with those of young and middle-aged individuals. Long-term serious insomnia not only affects the quality of life of patients but also increases the risk of some diseases and mortality. The mechanism of age-related changes in sleep patterns is not fully understood, and whether insomnia is a normal part of aging remains unclear. Telomeres are the ends of eukaryotic chromosomes that protect chromosome ends, maintain genome stability during transcription, and play a central role in the control of cell and body aging. Shortening of telomere length or changes in telomere structure can eventually lead to replicative senescence in cells and chromosomal instability, which are both markers of senescence. Aging is an inevitable consequence of life. In most organisms, the rate of aging is inversely proportional to average life span. Aging is also the biggest risk factor for cancer, neurodegeneration and cardiovascular diseases. Two studies were conducted on the relationship between insomnia and telomere length and aging, however, a systematic review of such studies is lacking. This paper will elaborate three aspects, namely, influence of insomnia on telomere length, significance of telomere length on aging and the effects of insomnia on aging.
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Key words:
- Insomnia /
- Telomere length /
- Aging
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[1] DONALD W B, JON E G. DSM-5® Guidebook: The Essential Companion to the Diagnostic and Statistical Manual of Mental Disorders[M]. 5th ed. Arlington, VA, US: American Psychiatric Publishing, 2014. [2] RIEMANN D, SPIEGELHALDER K, FEIGE B, et al. The hyperarousal model of insomnia: a review of the concept and its evidence[J]. Sleep Med Rev, 2010: 14(1): 19-31. doi: 10.1016/j.smrv.2009.04.002 [3] WATSON J D. Origin of concatemeric T7 DNA[J]. Nat New Biol, 1972, 239(94): 197-201. doi: 10.1038/newbio239197a0 [4] AGUADO J, SOLA-CARVAJAL A, CANCILA V, et al. Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson-Gilford Progeria Syndrome[J]. Nat Commun, 2019, 10(1): 4990. doi: 10.1038/s41467-019-13018-3 [5] LIU J, WANG L, WANG Z, et al. Roles of telomere biology in cell senescence, replicative and chronological ageing[J]. Cells, 2019, 8(1): 54. doi: 10.3390/cells8010054 [6] PRATHER A A, PUTERMAN E, LIN J, et al. Shorter leukocyte telomere length in midlife women with poor sleep quality[J]. J Aging Res, 2011, 2011: 721390. DOI: 10.4061/2011/721390. [7] JACKOWSKA M, HAMER M, CARVALHO L A, et al. Short sleep duration is associated with shorter telomere length in healthy men: findings from the Whitehall Ⅱ cohort study[J]. PLoS One, 2012, 7(10): e47292. DOI: 10.1371/journal.pone.0047292. [8] LIANG G, SCHEMHAMMER E, QI L, et al. Association between rotating night shifts, sleep duration, and telomere length in women[J]. PLoS One, 2011, 6(8): e23462. DOI: 10.1371/journal.pone.0023462. [9] CRIBBET M R, CARLISLE M, CAWTHON R M, et al. Cellular aging and restorative processes: subjective sleep quality and duration moderate the association between age and telomere length in a sample of middle-aged and older adults[J]. Sleep, 2014, 37(1): 65-70. doi: 10.5665/sleep.3308 [10] IRWIN M R, OLMSTEAD R, CARROLL J E. Sleep disturbance, sleep duration, and inflammation: a systematic review and meta-analysis of cohort studies and experimental sleep deprivation[J]. Biol Psychiatry, 2016, 80(1): 40-52. doi: 10.1016/j.biopsych.2015.05.014 [11] TEMPAKU P F, MAZZOTTI D R, TUFIK S. Telomere length as a marker of sleep loss and sleep disturbances: a potential link between sleep and cellular senescence[J]. Sleep Med, 2015, 16(5): 559-563. doi: 10.1016/j.sleep.2015.02.519 [12] WYNCHANK D, BIJLENGA D, PENNINX B W. Delayed sleep-onset and biological age: late sleep-onset is associated with shorter telomere length[J]. Sleep, 2019, 42(10): zsz139. DOI: 10.1093/sleep/zsz139. [13] ZHANG X, WANG Y, ZHAO R. Folic Acid Supplementation Suppresses Sleep Deprivation-Induced Telomere Dysfunction and Senescence-Associated Secretory Phenotype (SASP)[J]. Oxid Med Cell Longev, 2019, 2019: 4569614. DOI: 10.1155/2019/4569614. [14] ILOABUCHI C, INNES K E, SAMBAMOORTHI U. Association of sleep quality with telomere length, a marker of cellular aging: a retrospective cohort study of older adults in the United States[J]. Sleep Health, 2020, 6(4): 513-521. doi: 10.1016/j.sleh.2019.12.003 [15] LÓPEZ-OTÍN C, BLASCO M A, PARTRIDGE L, et al. The hallmarks of aging[J]. Cell, 2013, 153(6): 1194-217. doi: 10.1016/j.cell.2013.05.039 [16] BIRCH J, GIL J. Senescence and the SASP: many therapeutic avenues[J]. Genes Dev, 2020, 34(23-24): 1565-1576. doi: 10.1101/gad.343129.120 [17] AGUIAR-OLIVEIRA M H, BARTKE A. Growth Hormone Deficiency: health and Longevity[J]. Endocr Rev, 2019, 40(2): 575-601. doi: 10.1210/er.2018-00216 [18] KANDHAYA-PILLAI R, MIRO-MUR F, ALIJOTAS-REIG J, et al. TNF α-senescence initiates a STAT-dependent positive feedback loop, leading to a sustained interferon signature, DNA damage, and cytokine secretion[J]. Aging (Albany NY), 2017, 9(11): 2411-2435. [19] KIRKLAND J L, TCHKONIA T. Cellular senescence: a translational perspective[J]. EbioMedicine, 2017, 21: 21-28. doi: 10.1016/j.ebiom.2017.04.013 [20] TCHKONIA T, KIRKLAND J L. Aging, Cell senescence, and chronic disease: emerging therapeutic strategies[J]. JAMA, 2018, 320(13): 1319-1320. doi: 10.1001/jama.2018.12440 [21] NATH K A, O'BRIEN D R, CROATT A J, et al. The murine dialysis fistula model exhibits a senescence phenotype: pathobiological mechanisms and therapeutic potential[J]. Am J Physiol Renal Physiol, 2018, 315(5): F1493-F1499. doi: 10.1152/ajprenal.00308.2018 [22] IMAI J. β-Cell senescence in the pathogenesis of type 2 diabetes[J]. J Diabetes Investig, 2020, 11(2): 284-286. doi: 10.1111/jdi.13162 [23] PARIKH P, BRITT R D, MANLOVE L J, et al. Hyperoxia-induced cellular senescence in fetal airway smooth muscle cells[J]. Am J Respir Cell Mol Biol, 2019, 61(1): 51-60. doi: 10.1165/rcmb.2018-0176OC [24] PALMER A K, GUSTAFSON B, KIRKLAND J L, et al. Cellular senescence: at the nexus between ageing and diabetes[J]. Diabetologia, 2019, 62(10): 1835-1841. doi: 10.1007/s00125-019-4934-x [25] ANDERSON R, LAGNADO A, MAGGIORANI D, et al. Length-independent telomere damage drives post-mitotic cardiomyocyte senescence[J]. EMBO J, 2019, 38(5): e100492. DOI: 10.15252/embj.2018100492. [26] DE CECCO M, ITO T, PETRASHEN A P, et al. L1 drives IFN in senescent cells and promotes age-associated inflammation[J]. Nature, 2019, 566(7742): 73-78. doi: 10.1038/s41586-018-0784-9 [27] PALMER A K, XU M, ZHU Y, et al. Targeting senescent cells alleviates obesity-induced metabolic dysfunction[J]. Aging Cell, 2019, 18(3): e12950. doi: 10.1111/acel.12950 [28] WANG Y B, LIU Y L, CHEN E M, et al. The role of mitochondrial dysfunction in mesenchymal stem cell senescence[J]. Cell Tissue Res, 2020, 382(3): 457-462. doi: 10.1007/s00441-020-03272-z [29] JOHNSON G S, RAJENDRAN P, DASHWOOD R H. CCAR1 and CCAR2 as gene chameleons with antagonistic duality: preclinical, human translational, and mechanistic basis[J]. Cancer Sci, 2020, 111(10): 3416-3425. doi: 10.1111/cas.14579 [30] LUKÁŠOVÁ E, KOVA$ \ddot{{\rm{R}}}$ÍK A, KOZUBEK S. Consequences of lamin B1 and lamin B receptor downregulation in Senescence[J]. Cells, 2018, 7(2): 11. doi: 10.3390/cells7020011 [31] HAYFLICK L, MOORHEAD P S. The serial cultivation of human diploid cell strains[J]. Exp Cell Res, 1961, 25: 585-621. doi: 10.1016/0014-4827(61)90192-6 [32] HOU Y J, DAN X L, BABBAR M, et al. Ageing as a risk factor for neurodegenerative disease[J]. Nat Rev Neurol, 2019, 15(10): 565-581. doi: 10.1038/s41582-019-0244-7 [33] DOU Z X, GHOSH K, VIZIOLI M G, et al. Cytoplasmic chromatin triggers inflammation in senescence and cancer[J]. Nature, 2017, 550(7676): 402-406. doi: 10.1038/nature24050 [34] GUDE N A, BROUGHTON K M, FIROUZI F, et al. Cardiac ageing: extrinsic and intrinsic factors in cellular renewal and senescence[J]. Nat Rev Cardiol, 2018, 15(9): 523-542. doi: 10.1038/s41569-018-0061-5 [35] KHOSLA S, FARR J N, TCHKONIA T, et al. The role of cellular senescence in ageing and endocrine disease[J]. Nat Rev Endocrinol, 2020, 16(5): 263-275. doi: 10.1038/s41574-020-0335-y [36] ADAMS P D, JASPER H, RUDOLPH K L. Aging-induced stem cell mutations as drivers for disease and cancer[J]. Cell Stem Cell, 2015, 16(6): 601-12. doi: 10.1016/j.stem.2015.05.002 [37] MURAKI K, MURNANE J P. The DNA damage response at dysfunctional telomeres, and at interstitial and subtelomeric DNA double-strand breaks[J]. Genes Genet Syst, 2018, 92: 135-152. [38] TRIPATHY B K, PAL K, SHABRISH S, et al. A new perspective on the origin of dna double-strand breaks and its implications for ageing[J]. Genes (Basel), 2021, 12(2): 163. doi: 10.3390/genes12020163 [39] YIN J W, JIN X L, SHAN Z L, et al. Relationship of sleep duration with all-cause mortality and cardiovascular events: a systematic review and dose-response meta-analysis of prospective cohort studies[J]. J Am Heart Assoc, 2017, 6(9): e005947. DOI: 10.1161/JAHA.117.005947. [40] TAYLOR D J, MALLORY L J, LICHSTEIN K L, et al. Comorbidity of chronic insomnia with medical problems[J]. Sleep, 2007, 30(2): 213-218. doi: 10.1093/sleep/30.2.213 [41] 王羚入, 符晓艳, 王华, 等. 脑梗死后抑郁发生与人文因素、血管危险因素及卒中特点的相关性研究[J]. 中华全科医学, 2017, 15(2): 286-288. doi: 10.16766/j.cnki.issn.1674-4152.2017.02.031WANG L R, FU X Y, WANG H, et al. Association of post-stroke depression with demographic factors, vascular risk factors and stroke features in Chinese elderly population[J]. Chinese Journal of General Practice, 2017, 15(2): 286-288. doi: 10.16766/j.cnki.issn.1674-4152.2017.02.031 [42] GROSBELLET E, ZAHN S, ARRIVÉ M, et al. Circadian desynchronization triggers premature cellular aging in a diurnal rodent[J]. FASEB J, 2015, 29(12): 4794-4803. doi: 10.1096/fj.14-266817 [43] CHEN W D, WEN M S, SHIE S S, et al. The circadian rhythm controls telomeres and telomerase activity[J]. Biochem Biophys Res Commun, 2014, 451(3): 408-414. doi: 10.1016/j.bbrc.2014.07.138 [44] BIELAK-ZMIJEWSKA A, MOSIENIAK G, SIKORA E. Is DNA damage indispensable for stress-induced senescence?[J]. Mech Ageing Dev, 2018, 170: 13-21. doi: 10.1016/j.mad.2017.08.004 [45] FULOP T, LARBI A, DUPUIS G, et al. Immunosenescence and inflamm-aging as two sides of the same coin: friends or foes?[J]. Front Immunol, 2018, 8: 1960. doi: 10.3389/fimmu.2017.01960 [46] ARNARDOTTIR E S, NIKONOVA E V, SHOCKLEY K R, et al. Blood-gene expression reveals reduced circadian rhythmicity in individuals resistant to sleep deprivation[J]. Sleep, 2014, 37(10): 1589-1600. doi: 10.5665/sleep.4064 [47] HOLTH J K, FRITSCHI S K, WANG C, et al. The sleep-wake cycle regulates brain interstitial fluid tau in mice and CSF tau in humans[J]. Science, 2019, 363(6429): 880-884. doi: 10.1126/science.aav2546 [48] KELLY M R, ROBBINS R, MARTIN J L. Delivering cognitive behavioral therapy for insomnia in military personnel and veterans[J]. Sleep Med Clin, 2019, 14(2): 199-208. doi: 10.1016/j.jsmc.2019.01.003
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