留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

失眠与端粒长度和衰老的相关性研究进展

潘贤丽 苏增锋

潘贤丽, 苏增锋. 失眠与端粒长度和衰老的相关性研究进展[J]. 中华全科医学, 2023, 21(3): 481-484. doi: 10.16766/j.cnki.issn.1674-4152.002912
引用本文: 潘贤丽, 苏增锋. 失眠与端粒长度和衰老的相关性研究进展[J]. 中华全科医学, 2023, 21(3): 481-484. doi: 10.16766/j.cnki.issn.1674-4152.002912
PAN Xianli, SU Zengfeng. Correlation between insomnia and telomere length and aging[J]. Chinese Journal of General Practice, 2023, 21(3): 481-484. doi: 10.16766/j.cnki.issn.1674-4152.002912
Citation: PAN Xianli, SU Zengfeng. Correlation between insomnia and telomere length and aging[J]. Chinese Journal of General Practice, 2023, 21(3): 481-484. doi: 10.16766/j.cnki.issn.1674-4152.002912

失眠与端粒长度和衰老的相关性研究进展

doi: 10.16766/j.cnki.issn.1674-4152.002912
基金项目: 

安徽省教育厅高校自然科学研究重点项目 KJ2020A0189

安徽医科大学校科研基金项目 2020xkj219

详细信息
    通讯作者:

    苏增锋, E-mail:suzengfeng@163.com

  • 中图分类号: R592

Correlation between insomnia and telomere length and aging

  • 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。

     

  • [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.1674-4152.2017.02.031

    WANG 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
  • 加载中
计量
  • 文章访问数:  334
  • HTML全文浏览量:  198
  • PDF下载量:  22
  • 被引次数: 0
出版历程
  • 收稿日期:  2022-01-12
  • 网络出版日期:  2023-04-19

目录

    /

    返回文章
    返回