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Telomere Homeostasis in Ageing Related Pathologies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 8862

Special Issue Editor


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Guest Editor
Institute of Molecular Biology and Pathology, National Research Council, Rome, Italy
Interests: telomeres; telomerase; PARP1 inhibitors; G-quadruplex ligands; cancer and aging

Special Issue Information

Dear Colleagues,

Telomere homeostasis is essential to preserve the regenerative capacity of adult stem cells during aging and for the safeguard of genome stability during cell senescence. The alteration of telomere homeostasis is at the crossroad between senescence and cancer, and is also a biomarker for stress and inflammation response. Telomere homeostasis includes the maintenance of telomere length, the conservation of the epigenetic status of the telomeric and subtelomeric region, and the ability to suppress DNA damage response (DDR). Telomeric DNA repeats provide a molecular scaffold for structural proteins and enzymes, whose number is constantly growing. More interestingly, some “telomere-specific” proteins were recently found in non-telomeric loci. This has raised new questions about the impact of telomere dynamics on the whole DNA metabolism.

This Special Issue of the International Journal of Molecular Sciences welcomes commentary, research, or review articles regarding the basic mechanisms of telomere metabolism, preclinical/clinical evaluation of telomere targeting agents, or validation of telomere-related parameters as biomarkers in aging-related pathologies.

Dr. Erica Salvati
Guest Editor

Manuscript Submission Information

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Keywords

  • telomeres
  • telomerase
  • ALT
  • DNA damage response
  • DNA replication
  • PARP1
  • G-quadruplex ligands
  • cancer
  • aging

Published Papers (2 papers)

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Review

17 pages, 969 KiB  
Review
Telomere Shortening and Its Association with Cell Dysfunction in Lung Diseases
by Andy Ruiz, Julio Flores-Gonzalez, Ivette Buendia-Roldan and Leslie Chavez-Galan
Int. J. Mol. Sci. 2022, 23(1), 425; https://doi.org/10.3390/ijms23010425 - 31 Dec 2021
Cited by 12 | Viewed by 4534
Abstract
Telomeres are localized at the end of chromosomes to provide genome stability; however, the telomere length tends to be shortened with each cell division inducing a progressive telomere shortening (TS). In addition to age, other factors, such as exposure to pollutants, diet, stress, [...] Read more.
Telomeres are localized at the end of chromosomes to provide genome stability; however, the telomere length tends to be shortened with each cell division inducing a progressive telomere shortening (TS). In addition to age, other factors, such as exposure to pollutants, diet, stress, and disruptions in the shelterin protein complex or genes associated with telomerase induce TS. This phenomenon favors cellular senescence and genotoxic stress, which increases the risk of the development and progression of lung diseases such as idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, SARS-CoV-2 infection, and lung cancer. In an infectious environment, immune cells that exhibit TS are associated with severe lymphopenia and death, whereas in a noninfectious context, naïve T cells that exhibit TS are related to cancer progression and enhanced inflammatory processes. In this review, we discuss how TS modifies the function of the immune system cells, making them inefficient in maintaining homeostasis in the lung. Finally, we discuss the advances in drug and gene therapy for lung diseases where TS could be used as a target for future treatments. Full article
(This article belongs to the Special Issue Telomere Homeostasis in Ageing Related Pathologies)
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15 pages, 1178 KiB  
Review
Telomere Attrition and Clonal Hematopoiesis of Indeterminate Potential in Cardiovascular Disease
by Yi-Chun Huang and Chao-Yung Wang
Int. J. Mol. Sci. 2021, 22(18), 9867; https://doi.org/10.3390/ijms22189867 - 13 Sep 2021
Cited by 5 | Viewed by 3719
Abstract
Clinical evidence suggests that conventional cardiovascular disease (CVD) risk factors cannot explain all CVD incidences. Recent studies have shown that telomere attrition, clonal hematopoiesis of indeterminate potential (CHIP), and atherosclerosis (telomere–CHIP–atherosclerosis, TCA) evolve to play a crucial role in CVD. Telomere dynamics and [...] Read more.
Clinical evidence suggests that conventional cardiovascular disease (CVD) risk factors cannot explain all CVD incidences. Recent studies have shown that telomere attrition, clonal hematopoiesis of indeterminate potential (CHIP), and atherosclerosis (telomere–CHIP–atherosclerosis, TCA) evolve to play a crucial role in CVD. Telomere dynamics and telomerase have an important relationship with age-related CVD. Telomere attrition is associated with CHIP. CHIP is commonly observed in elderly patients. It is characterized by an increase in blood cell clones with somatic mutations, resulting in an increased risk of hematological cancer and atherosclerotic CVD. The most common gene mutations are DNA methyltransferase 3 alpha (DNMT3A), Tet methylcytosine dioxygenase 2 (TET2), and additional sex combs-like 1 (ASXL1). Telomeres, CHIP, and atherosclerosis increase chronic inflammation and proinflammatory cytokine expression. Currently, their epidemiology and detailed mechanisms related to the TCA axis remain incompletely understood. In this article, we reviewed recent research results regarding the development of telomeres and CHIP and their relationship with atherosclerotic CVD. Full article
(This article belongs to the Special Issue Telomere Homeostasis in Ageing Related Pathologies)
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