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Telomeres in Development, Senescence and Genome Instability: 2nd Edition

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 June 2026) | Viewed by 3281

Editor


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Guest Editor
Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
Interests: telomere; stem cells; embryonic stem cells; induced pluripotent stem cells; cancer stem cells

Special Issue Information

Dear Colleagues,

Telomere biology, as a special area of biology, was identified1971–1973 by Alexey Olovnikov (1936–2022) through his research on the under-replication of the ends of linear chromosomes. In his telomeric theory of aging, Alexey Olovnikov also determined the key roles of telomeres in various fundamental processes, such as cell death, cancer, and aging. Indeed, telomere functions are closely linked to many cellular processes, in particular through telomere signalling mechanisms, although their molecular basis remains poorly understood. Telomere shortening and telomere dysfunction are hallmarks of cellular senescence, aging and oncogenesis, highlighting the importance of the telomere state in genome stability. This Special Issue will compile research and methodological articles, reviews, and the opinions of authors regarding the diverse and fascinating field of telomere biology.

Topics include, but are not limited to, the following:

  • Telomere disorders and cell death;
  • Telomere factors as therapeutic targets in cancer;
  • Telomeres and genome stability;
  • Epigenetics of telomeres in development and aging;
  • Mechanisms of telomere signalling;
  • Telomeres in aging and senescence;
  • Telomeropathies and laminopathies;
  • Telomere protection mechanisms in development;
  • Telomeres in non-model organisms;
  • Telomere length control in germline and stem cells;
  • Novel methods of telomere analysis.

Dr. Michal Zalzman
Guest Editor

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Keywords

  • telomere disorders and cell death
  • telomere factors as therapeutic targets in cancer
  • telomeres and genome stability
  • telomeres in aging and senescence

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Published Papers (2 papers)

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Review

35 pages, 1161 KB  
Review
Impact of Maternal Lifetime Stress on Offspring Biological Aging: A Systematic Review and Meta-Analysis of Observational Studies
by María Loreto Muñoz Venegas, Miriam Shasa Quiccione, Sukshma Sharma, Francesco Gianfagna, Francesca Bracone, Paola De Domenico, Alfonsina Tirozzi, Chiara Cerletti, Maria Benedetta Donati, Giovanni de Gaetano, Licia Iacoviello and Alessandro Gialluisi
Int. J. Mol. Sci. 2026, 27(7), 3019; https://doi.org/10.3390/ijms27073019 - 26 Mar 2026
Viewed by 1261
Abstract
Maternal stress during lifetime and pregnancy may influence offspring epigenetic age, impacting long-term health. We conducted a systematic review and meta-analysis of associations between maternal stress and epigenetic aging markers: telomere length (TL) and DNA methylation (DNAm) age acceleration. The systematic search was [...] Read more.
Maternal stress during lifetime and pregnancy may influence offspring epigenetic age, impacting long-term health. We conducted a systematic review and meta-analysis of associations between maternal stress and epigenetic aging markers: telomere length (TL) and DNA methylation (DNAm) age acceleration. The systematic search was performed according to PRISMA guidelines and registered on PROSPERO (ref. CRD42023474640). Fixed and random effect meta-analyses were carried out, stratified by stress type and marker type (TL, DNAm). Sixteen studies met inclusion criteria; 12 were meta-analyzed (10 TL, 2 DNAm). Due to high heterogeneity, restricted maximum likelihood meta-analysis suggested significant inverse associations between maternal stress and offspring TL. Perceived stress was associated with shorter TL (p-value = 7 × 10−4, β = −0.085, 95%CI [−0.135, −0.036]), as was lifetime stress/trauma (p-value = 0.01, β = −0.209, 95%CI [−0.370, −0.049]). In contrast, maternal stress showed no significant associations with DNAm age acceleration (p-value = 0.32). Both perceived maternal stress and maternal stress were associated with shorter offspring TL, suggesting that stress exposure across the maternal lifespan influences offspring biological aging markers. No significant association was observed with DNAm-based aging clocks. Further studies with larger sample sizes and more homogeneous settings are needed to confirm and expand upon our observations. Full article
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15 pages, 590 KB  
Review
Molecular Mechanisms of Accelerated Ageing in Geriatric Depression: Interplay of Telomere Attrition, Mitochondrial Dysfunction and Cellular Senescence
by Pratibha Revi Shanker and Rajkumar Dorajoo
Int. J. Mol. Sci. 2026, 27(3), 1613; https://doi.org/10.3390/ijms27031613 - 6 Feb 2026
Cited by 5 | Viewed by 1357
Abstract
Late-life depression is a prevalent and debilitating disorder. It differs significantly from depression in younger adults and often co-occurs with cognitive decline and increased physical frailty. This narrative review explores the role of accelerated biological ageing in late-life depression. We examine evidence linking [...] Read more.
Late-life depression is a prevalent and debilitating disorder. It differs significantly from depression in younger adults and often co-occurs with cognitive decline and increased physical frailty. This narrative review explores the role of accelerated biological ageing in late-life depression. We examine evidence linking three interconnected processes, namely telomere attrition, mitochondrial dysfunction and cellular senescence, to the pathophysiology of late-life depression. Excessive attrition of telomeres may serve as a biomarker of accumulated stress and cellular ageing. Mitochondrial dysfunction not only reduces energy production but also promotes oxidative stress and inflammation that increase neuroinflammatory pathways and synaptic loss. Increased cellular senescence further induces senescence-associated secretory phenotype factors that drive chronic inflammation and neuronal loss. Together, these processes create a cycle of cellular stress, persistent inflammation and damage to brain circuits involved in late-life depression. We additionally highlight potential limitations in current findings and propose a roadmap for future research to better elucidate the mechanistic dysfunction of late-life depression. These include the need for evaluation in long-term prospective cohort studies, improved tools to better correlate blood-based markers with changes in disease-relevant brain tissues and regions, and trials that test treatment and lifestyle modifications that are targeted at ageing biomarkers. Full article
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