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      Healthy aging and disease: role for telomere biology?

      review-article
      Author(s): * , * , †
      Publication date (Electronic):
      Journal: Clinical Science (London, England : 1979)
      Publisher: Portland Press Ltd.
      Keywords: aging, Alzheimer's disease, atherosclerosis, heart failure, longevity, Parkinson's disease, telomerase, telomere, ACEI, angiotensin-converting enzyme inhibitor, AD, Alzheimer's disease, CHF, chronic heart failure, CRP, C-reactive protein, CVD, cardiovascular disease, DHA, docosahexaenoic acid, EPA, eicosapentaenoic acid, LDL, low-density lipoprotein, PBMC, peripheral blood mononuclear cell, PD, Parkinson's disease, SHR, spontaneous hypertensive rats, T1D, Type 1 diabetes, T2D, Type 2 diabetes, TERC, telomerase RNA component, TERRA, telomeric repeat-containing RNA, TERT, telomerase reverse transcriptase, TRF, telomeric repeat-binding factor

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          Abstract

          Aging is a biological process that affects most cells, organisms and species. Human aging is associated with increased susceptibility to a variety of chronic diseases, including cardiovascular disease, Type 2 diabetes, neurological diseases and cancer. Despite the remarkable progress made during the last two decades, our understanding of the biology of aging remains incomplete. Telomere biology has recently emerged as an important player in the aging and disease process.

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          Most cited references135

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          Oxidative stress shortens telomeres.

          Thomas von Zglinicki (2002)
          Telomeres in most human cells shorten with each round of DNA replication, because they lack the enzyme telomerase. This is not, however, the only determinant of the rate of loss of telomeric DNA. Oxidative damage is repaired less well in telomeric DNA than elsewhere in the chromosome, and oxidative stress accelerates telomere loss, whereas antioxidants decelerate it. I suggest here that oxidative stress is an important modulator of telomere loss and that telomere-driven replicative senescence is primarily a stress response. This might have evolved to block the growth of cells that have been exposed to a high risk of mutation.
          Article 0 comments Cited 767 times – based on 0 reviews     Review now
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            Telomeres and human disease: ageing, cancer and beyond.

            Maria A. Blasco (2005)
            Telomere length and telomerase activity are important factors in the pathobiology of human disease. Age-related diseases and premature ageing syndromes are characterized by short telomeres, which can compromise cell viability, whereas tumour cells can prevent telomere loss by aberrantly upregulating telomerase. Altered functioning of both telomerase and telomere-interacting proteins is present in some human premature ageing syndromes and in cancer, and recent findings indicate that alterations that affect telomeres at the level of chromatin structure might also have a role in human disease. These findings have inspired a number of potential therapeutic strategies that are based on telomerase and telomeres.
            Article 0 comments Cited 456 times – based on 0 reviews     Review now
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              Obesity, cigarette smoking, and telomere length in women.

              A Valdes, T. Andrew, J. P. Gardner … (2005)
              Obesity and smoking are important risk factors for many age-related diseases. Both are states of heightened oxidative stress, which increases the rate of telomere erosion per replication, and inflammation, which enhances white blood cell turnover. Together, these processes might accelerate telomere erosion with age. We therefore tested the hypothesis that increased body mass and smoking are associated with shortened telomere length in white blood cells. We investigated 1122 white women aged 18-76 years and found that telomere length decreased steadily with age at a mean rate of 27 bp per year. Telomeres of obese women were 240 bp shorter than those of lean women (p=0.026). A dose-dependent relation with smoking was recorded (p=0.017), and each pack-year smoked was equivalent to an additional 5 bp of telomere length lost (18%) compared with the rate in the overall cohort. Our results emphasise the pro-ageing effects of obesity and cigarette smoking.
              Article 0 comments Cited 402 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Sci (Lond)
                Journal ID (pmc): cls
                Journal ID (publisher-id): CS
                Title: Clinical Science (London, England : 1979)
                Publisher: Portland Press Ltd.
                ISSN (Print): 0143-5221
                ISSN (Electronic): 1470-8736
                Publication date (Electronic): 28 January 2011
                Publication date (Print): 1 May 2011
                Volume: 120
                Issue: Pt 10
                Pages: 427-440
                Affiliations
                *Department of Pediatrics, Georgia Prevention Institute, Medical College of Georgia, Augusta, GA30912, U.S.A
                †Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands
                Author notes
                Correspondence: Dr Haidong Zhu (email hzhu@ 123456mail.mcg.edu ) or Dr Pim van der Harst ( p.van.der.harst@ 123456thorax.umcg.nl ).
                Article
                Publisher ID: cs1200427
                DOI: 10.1042/CS20100385
                PMC ID: 3035527
                PubMed ID: 21271986
                SO-VID: a4dcd043-f403-4848-9580-3aa7551d9527
                Copyright © © 2011 The Author(s) The author(s) has paid for this article to be freely available under the terms of the Creative Commons Attribution Non-Commercial Licence (http://creativecommons.org/licenses/by-nc/2.5/) which permits unrestricted non-commercial use, distribution and reproduction in any medium, provided the original work is properly cited.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 27 July 2010
                Date revision received : 27 October 2010
                Date accepted : 22 November 2010
                Page count
                Figures: 3, References: 159, Pages: 14
                Categories
                Subject: Review Article
                Subject: S1
                Subject: S5

                ScienceOpen disciplines: Medicine
                Keywords: terc, telomerase rna component,ldl, low-density lipoprotein,dha, docosahexaenoic acid,epa, eicosapentaenoic acid,heart failure,shr, spontaneous hypertensive rats,terra, telomeric repeat-containing rna,longevity,trf, telomeric repeat-binding factor,t2d, type 2 diabetes,chf, chronic heart failure,acei, angiotensin-converting enzyme inhibitor,tert, telomerase reverse transcriptase,alzheimer's disease,cvd, cardiovascular disease,pbmc, peripheral blood mononuclear cell,aging,atherosclerosis,parkinson's disease,t1d, type 1 diabetes,pd, parkinson's disease,telomere,ad, alzheimer's disease,telomerase,crp, c-reactive protein
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: terc, telomerase rna component, ldl, low-density lipoprotein, dha, docosahexaenoic acid, epa, eicosapentaenoic acid, heart failure, shr, spontaneous hypertensive rats, terra, telomeric repeat-containing rna, longevity, trf, telomeric repeat-binding factor, t2d, type 2 diabetes, chf, chronic heart failure, acei, angiotensin-converting enzyme inhibitor, tert, telomerase reverse transcriptase, alzheimer's disease, cvd, cardiovascular disease, pbmc, peripheral blood mononuclear cell, aging, atherosclerosis, parkinson's disease, t1d, type 1 diabetes, pd, parkinson's disease, telomere, ad, alzheimer's disease, telomerase, crp, c-reactive protein

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