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The Role of Telomere Biology in Aging and Human Disease...
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The Role of Telomere Biology in Aging and Human Disease II

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: closed (15 April 2022) | Viewed by 17495

Special Issue Editors

Prof. Dr. Rajiv Kumar

E-Mail Website
Guest Editor
Division of Functional Genome Analysis, German Cancer Research Center, Im Neunheimer Feld 580, 69120 Heidelberg, Germany
Interests: cancer genetics; somatic mutations; telomerase
Special Issues, Collections and Topics in MDPI journals
Dr. David Gilley

E-Mail Website
Former Collection Editor
Department of Chemistry and Applied Biological Sciences, South Dakota School of Mines & Technology, Rapid City, SD 57701, USA
Interests: telomere; telomerase; genomic instability; cancer; DNA damage response; stem/progenitor cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ground-breaking fundamental work in identifying and discovering the basic role of telomeres and telomerase has laid the foundation for a plethora of evidence that telomere biology plays multiple crucial roles in human health. Telomere biology has been implicated in major human biological processes from aging to cancer, cardiovascular disease, numerous heritable disorders, and other human diseases and disease-resistant states.

In this Special Issue of Cells, we invite your contributions, either in the form of original research articles, reviews, or shorter perspective articles on all aspects related to the theme of “The Role of Telomere Biology in Aging and Human Disease”. Articles with mechanistic and functional insights from a cell and molecular biological perspective are especially welcome. Relevant topics include but are not limited to:

  • Telomere biology and cancer;
  • Telomere biology and the environment;
  • Telomere dynamics in stem and progenitor cells;
  • Heritable telomere disorders;
  • Modes of telomere dysfunction in human systems;
  • Human telomere biology;
  • Telomeres and aging;
  • The role of telomeres in cardiovascular disease;
  • Telomere biology and disease resistance (including tumor suppression) pathways;
  • Telomere biology and the DNA damage response.

Prof. Dr. Rajiv Kumar
Dr. David Gilley
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Telomere
  • Telomerase
  • Cancer
  • Aging
  • Heritable disorders

Related Special Issue

Published Papers (4 papers)

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Research

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16 pages, 4767 KiB  
Article
Sir4 Deficiency Reverses Cell Senescence by Sub-Telomere Recombination
by Jun Liu, Xiaojing Hong, Lihui Wang, Chao-Ya Liang and Jun-Ping Liu
Cells 2021, 10(4), 778; https://doi.org/10.3390/cells10040778 - 01 Apr 2021
Cited by 4 | Viewed by 2463
Abstract
Telomere shortening results in cellular senescence and the regulatory mechanisms remain unclear. Here, we report that the sub-telomere regions facilitate telomere lengthening by homologous recombination, thereby attenuating senescence in yeast Saccharomyces cerevisiae. The telomere protein complex Sir3/4 represses, whereas Rif1 promotes, the [...] Read more.
Telomere shortening results in cellular senescence and the regulatory mechanisms remain unclear. Here, we report that the sub-telomere regions facilitate telomere lengthening by homologous recombination, thereby attenuating senescence in yeast Saccharomyces cerevisiae. The telomere protein complex Sir3/4 represses, whereas Rif1 promotes, the sub-telomere Y′ element recombination. Genetic disruption of SIR4 increases Y′ element abundance and rescues telomere-shortening-induced senescence in a Rad51-dependent manner, indicating a sub-telomere regulatory switch in regulating organismal senescence by DNA recombination. Inhibition of the sub-telomere recombination requires Sir4 binding to perinuclear protein Mps3 for telomere perinuclear localization and transcriptional repression of the telomeric repeat-containing RNA TERRA. Furthermore, Sir4 repression of Y′ element recombination is negatively regulated by Rif1 that mediates senescence-evasion induced by Sir4 deficiency. Thus, our results demonstrate a dual opposing control mechanism of sub-telomeric Y′ element recombination by Sir3/4 and Rif1 in the regulation of telomere shortening and cell senescence. Full article
(This article belongs to the Special Issue The Role of Telomere Biology in Aging and Human Disease II)
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8 pages, 1318 KiB  
Communication
TERC Variants Associated with Short Leukocyte Telomeres: Implication of Higher Early Life Leukocyte Telomere Attrition as Assessed by the Blood-and-Muscle Model
by Simon Toupance, Maria G. Stathopoulou, Alexandros M. Petrelis, Vesna Gorenjak, Carlos Labat, Tsung-Po Lai, Sophie Visvikis-Siest and Athanase Benetos
Cells 2020, 9(6), 1360; https://doi.org/10.3390/cells9061360 - 31 May 2020
Cited by 3 | Viewed by 2294
Abstract
Short leukocyte telomere length (LTL) is associated with atherosclerotic cardiovascular disease (ASCVD). Mendelian randomisation studies, using single nucleotide polymorphisms (SNPs) associated with short LTL, infer a causal role of LTL in ASCVD. Recent results, using the blood-and-muscle model, indicate that higher early life [...] Read more.
Short leukocyte telomere length (LTL) is associated with atherosclerotic cardiovascular disease (ASCVD). Mendelian randomisation studies, using single nucleotide polymorphisms (SNPs) associated with short LTL, infer a causal role of LTL in ASCVD. Recent results, using the blood-and-muscle model, indicate that higher early life LTL attrition, as estimated by the ratio between LTL and skeletal muscle telomere length (MTL), rather than short LTL at conception, as estimated by MTL, should be responsible of the ASCVD-LTL connection. We combined LTL and MTL measurements and SNPs profiling in 402 individuals to determine if 15 SNPs classically described as associated with short LTL at adult age were rather responsible for higher LTL attrition during early life than for shorter LTL at birth. Two of these SNPs (rs12696304 and rs10936599) were associated with LTL in our cohort (p = 0.027 and p = 0.025, respectively). These SNPs, both located on the TERC gene, were associated with the LTL/MTL ratio (p = 0.007 and p = 0.037, respectively), but not with MTL (p = 0.78 and p = 0.32 respectively). These results suggest that SNPs located on genes coding for telomere maintenance proteins may contribute to a higher LTL attrition during the highly replicative first years of life and have an impact later on the development of ASCVD. Full article
(This article belongs to the Special Issue The Role of Telomere Biology in Aging and Human Disease II)
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Review

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32 pages, 2217 KiB  
Review
Structural Features of Nucleoprotein CST/Shelterin Complex Involved in the Telomere Maintenance and Its Association with Disease Mutations
by Mohd. Amir, Parvez Khan, Aarfa Queen, Ravins Dohare, Mohamed F. Alajmi, Afzal Hussain, Asimul Islam, Faizan Ahmad and Md. Imtaiyaz Hassan
Cells 2020, 9(2), 359; https://doi.org/10.3390/cells9020359 - 04 Feb 2020
Cited by 26 | Viewed by 6296
Abstract
Telomere comprises the ends of eukaryotic linear chromosomes and is composed of G-rich (TTAGGG) tandem repeats which play an important role in maintaining genome stability, premature aging and onsets of many diseases. Majority of the telomere are replicated by conventional DNA replication, and [...] Read more.
Telomere comprises the ends of eukaryotic linear chromosomes and is composed of G-rich (TTAGGG) tandem repeats which play an important role in maintaining genome stability, premature aging and onsets of many diseases. Majority of the telomere are replicated by conventional DNA replication, and only the last bit of the lagging strand is synthesized by telomerase (a reverse transcriptase). In addition to replication, telomere maintenance is principally carried out by two key complexes known as shelterin (TRF1, TRF2, TIN2, RAP1, POT1, and TPP1) and CST (CDC13/CTC1, STN1, and TEN1). Shelterin protects the telomere from DNA damage response (DDR) and regulates telomere length by telomerase; while, CST govern the extension of telomere by telomerase and C strand fill-in synthesis. We have investigated both structural and biochemical features of shelterin and CST complexes to get a clear understanding of their importance in the telomere maintenance. Further, we have analyzed ~115 clinically important mutations in both of the complexes. Association of such mutations with specific cellular fault unveils the importance of shelterin and CST complexes in the maintenance of genome stability. A possibility of targeting shelterin and CST by small molecule inhibitors is further investigated towards the therapeutic management of associated diseases. Overall, this review provides a possible direction to understand the mechanisms of telomere borne diseases, and their therapeutic intervention. Full article
(This article belongs to the Special Issue The Role of Telomere Biology in Aging and Human Disease II)
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Other

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68 pages, 2290 KiB  
Systematic Review
Telomere Shortening and Psychiatric Disorders: A Systematic Review
by Pedro A. Pousa, Raquel M. Souza, Paulo Henrique M. Melo, Bernardo H. M. Correa, Tamires S. C. Mendonça, Ana Cristina Simões-e-Silva and Débora M. Miranda
Cells 2021, 10(6), 1423; https://doi.org/10.3390/cells10061423 - 07 Jun 2021
Cited by 27 | Viewed by 5279
Abstract
Telomeres are aging biomarkers, as they shorten while cells undergo mitosis. The aim of this study was to evaluate whether psychiatric disorders marked by psychological distress lead to alterations to telomere length (TL), corroborating the hypothesis that mental disorders might have a deeper [...] Read more.
Telomeres are aging biomarkers, as they shorten while cells undergo mitosis. The aim of this study was to evaluate whether psychiatric disorders marked by psychological distress lead to alterations to telomere length (TL), corroborating the hypothesis that mental disorders might have a deeper impact on our physiology and aging than it was previously thought. A systematic search of the literature using MeSH descriptors of psychological distress (“Traumatic Stress Disorder” or “Anxiety Disorder” or “depression”) and telomere length (“cellular senescence”, “oxidative stress” and “telomere”) was conducted on PubMed, Cochrane Library and ScienceDirect databases. A total of 56 studies (113,699 patients) measured the TL from individuals diagnosed with anxiety, depression and posttraumatic disorders and compared them with those from healthy subjects. Overall, TL negatively associates with distress-related mental disorders. The possible underlying molecular mechanisms that underly psychiatric diseases to telomere shortening include oxidative stress, inflammation and mitochondrial dysfunction linking. It is still unclear whether psychological distress is either a cause or a consequence of telomere shortening. Full article
(This article belongs to the Special Issue The Role of Telomere Biology in Aging and Human Disease II)
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