scholarly journals The Impact of Exercise on Telomere Length, DNA Methylation and Metabolic Footprints

Cells ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 153
Author(s):  
Sandra Haupt ◽  
Tobias Niedrist ◽  
Harald Sourij ◽  
Stephan Schwarzinger ◽  
Othmar Moser
Keyword(s):  
Dna Methylation ◽  
Telomere Length ◽  
Analytical Methods ◽  
Aging Process ◽  
Biological Process ◽  
Technical Expertise ◽  
Telomere Shortening ◽  
Underlying Mechanisms ◽  
High Level ◽  
The Impact

Aging as a major risk factor influences the probability of developing cancer, cardiovascular disease and diabetes, amongst others. The underlying mechanisms of disease are still not fully understood, but research suggests that delaying the aging process could ameliorate these pathologies. A key biological process in aging is cellular senescence which is associated with several stressors such as telomere shortening or enhanced DNA methylation. Telomere length as well as DNA methylation levels can be used as biological age predictors which are able to detect excessive acceleration or deceleration of aging. Analytical methods examining aging are often not suitable, expensive, time-consuming or require a high level of technical expertise. Therefore, research focusses on combining analytical methods which have the potential to simultaneously analyse epigenetic, genomic as well as metabolic changes.

scholarly journals Born to be young? Prenatal thyroid hormones increase early-life telomere length in wild collared flycatchers

2020 ◽  
Vol 16 (11) ◽  
pp. 20200364
Author(s):  
Antoine Stier ◽  
Bin-Yan Hsu ◽  
Coline Marciau ◽  
Blandine Doligez ◽  
Lars Gustafsson ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Telomere Length ◽  
Early Life ◽  
Copy Number ◽  
Growth Period ◽  
Mtdna Copy Number ◽  
Cross Sectional ◽  
Telomere Shortening ◽  
Underlying Mechanisms ◽  
Age At Birth

The underlying mechanisms of the lifelong consequences of prenatal environmental condition on health and ageing remain little understood. Thyroid hormones (THs) are important regulators of embryogenesis, transferred from the mother to the embryo. Since prenatal THs can accelerate early-life development, we hypothesized that this might occur at the expense of resource allocation in somatic maintenance processes, leading to premature ageing. Therefore, we investigated the consequences of prenatal TH supplementation on potential hallmarks of ageing in a free-living avian model in which we previously demonstrated that experimentally elevated prenatal TH exposure accelerates early-life growth. Using cross-sectional sampling, we first report that mitochondrial DNA (mtDNA) copy number and telomere length significantly decrease from early-life to late adulthood, thus suggesting that these two molecular markers could be hallmarks of ageing in our wild bird model. Elevated prenatal THs had no effect on mtDNA copy number but counterintuitively increased telomere length both soon after birth and at the end of the growth period (equivalent to offsetting ca 4 years of post-growth telomere shortening). These findings suggest that prenatal THs might have a role in setting the ‘biological' age at birth, but raise questions about the nature of the evolutionary costs of prenatal exposure to high TH levels.

scholarly journals Impact of telomerase ablation on organismal viability, aging, and tumorigenesis in mice lacking the DNA repair proteins PARP-1, Ku86, or DNA-PKcs

2004 ◽  
Vol 167 (4) ◽  
pp. 627-638 ◽  
Author(s):  
Silvia Espejel ◽  
Peter Klatt ◽  
Josiane Ménissier-de Murcia ◽  
Juan Martín-Caballero ◽  
Juana M. Flores ◽  
...  
Keyword(s):  
Dna Repair ◽  
Aging Process ◽  
Telomere Shortening ◽  
Age Related ◽  
Dna Repair Proteins ◽  
Telomere Function ◽  
Telomere Capping ◽  
The Impact ◽  
Parp 1 ◽  
Deficient Mice

The DNA repair proteins poly(ADP-ribose) polymerase-1 (PARP-1), Ku86, and catalytic subunit of DNA-PK (DNA-PKcs) have been involved in telomere metabolism. To genetically dissect the impact of these activities on telomere function, as well as organismal cancer and aging, we have generated mice doubly deficient for both telomerase and any of the mentioned DNA repair proteins, PARP-1, Ku86, or DNA-PKcs. First, we show that abrogation of PARP-1 in the absence of telomerase does not affect the rate of telomere shortening, telomere capping, or organismal viability compared with single telomerase-deficient controls. Thus, PARP-1 does not have a major role in telomere metabolism, not even in the context of telomerase deficiency. In contrast, mice doubly deficient for telomerase and either Ku86 or DNA-PKcs manifest accelerated loss of organismal viability compared with single telomerase-deficient mice. Interestingly, this loss of organismal viability correlates with proliferative defects and age-related pathologies, but not with increased incidence of cancer. These results support the notion that absence of telomerase and short telomeres in combination with DNA repair deficiencies accelerate the aging process without impacting on tumorigenesis.

scholarly journals Parallel telomere shortening in multiple body tissues owing to malaria infection

2016 ◽  
Vol 283 (1836) ◽  
pp. 20161184 ◽  
Author(s):  
Muhammad Asghar ◽  
Vaidas Palinauskas ◽  
Nadège Zaghdoudi-Allan ◽  
Gediminas Valkiūnas ◽  
Andrey Mukhin ◽  
...  
Keyword(s):  
Telomere Length ◽  
Quantitative Polymerase Chain Reaction ◽  
Telomere Shortening ◽  
Tissue Samples ◽  
Telomere Attrition ◽  
Body Tissues ◽  
Increased Risk ◽  
Avian Malaria Parasite ◽  
Systemic Stress ◽  
The Impact

Several studies have shown associations between shorter telomere length in blood and weakened immune function, susceptibility to infections, and increased risk of morbidity and mortality. Recently, we have shown that malaria accelerates telomere attrition in blood cells and shortens lifespan in birds. However, the impact of infections on telomere attrition in different body tissues within an individual is unknown. Here, we tested whether malarial infection leads to parallel telomere shortening in blood and tissue samples from different organs. We experimentally infected siskins ( Spinus spinus ) with the avian malaria parasite Plasmodium ashfordi , and used real-time quantitative polymerase chain reaction (PCR) to measure telomere length in control and experimentally infected siskins. We found that experimentally infected birds showed faster telomere attrition in blood over the course of infection compared with control individuals (repeatedly measured over 105 days post-infection (DPI)). Shorter telomeres were also found in the tissue of all six major organs investigated (liver, lungs, spleen, heart, kidney, and brain) in infected birds compared with controls at 105 DPI. To the best of our knowledge, this is the first study showing that an infectious disease results in synchronous telomere shortening in the blood and tissue cells of internal organs within individuals, implying that the infection induces systemic stress. Our results have far-reaching implications for understanding how the short-term effects of an infection can translate into long-term costs, such as organ dysfunction, degenerative diseases, and ageing.

scholarly journals Impact of Snoring on Telomere Shortening in Adolescents with Atopic Diseases

Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 766
Author(s):  
T.-S. (Keith) Tung ◽  
S. (Rosa) Wong ◽  
Hing-Wai Tsang ◽  
T. (Gilbert) Chua ◽  
Y.-T. (Dicky) Chan ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Telomere Length ◽  
Cellular Level ◽  
Buccal Swab ◽  
Atopic Diseases ◽  
Telomere Shortening ◽  
Cellular Marker ◽  
Significant Burden ◽  
History Of ◽  
The Impact

Atopic diseases can impose a significant burden on children and adolescents. Telomere length is a cellular marker of aging reflecting the impact of cumulative stress exposure on individual health. Since elevated oxidative stress and inflammation burden induced by chronic atopy and snoring may impact telomere length, this study aimed to investigate whether snoring would moderate the relationship between atopic diseases and telomere length in early adolescence. We surveyed 354 adolescents and their parents. Parents reported the adolescents’ history of atopic diseases, recent snoring history as well as other family sociodemographic characteristics. Buccal swab samples were also collected from the adolescents for telomere length determination. Independent and combined effects of atopic diseases and snoring on telomere length were examined. Among the surveyed adolescents, 174 were reported by parents to have atopic diseases (20 had asthma, 145 had allergic rhinitis, 53 had eczema, and 25 had food allergy). Shorter TL was found in participants with a history of snoring and atopic diseases (β = −0.34, p = 0.002) particularly for asthma (β = −0.21, p = 0.007) and allergic rhinitis (β = −0.22, p = 0.023). Our findings suggest that snoring in atopic patients has important implications for accelerated telomere shortening. Proper management of atopic symptoms at an early age is important for the alleviation of long-term health consequences at the cellular level.

scholarly journals Prenatal thyroid hormones accelerate postnatal growth and telomere shortening in wild great tits

2021 ◽  
Author(s):  
Bin-Yan Hsu ◽  
Nina Cossin-Sevrin ◽  
Antoine Stier ◽  
Suvi Ruuskanen
Keyword(s):  
Oxidative Stress ◽  
Thyroid Hormones ◽  
Telomere Length ◽  
Early Life ◽  
Later Life ◽  
Delayed Effect ◽  
Oxidative Stress Biomarkers ◽  
Term Survival ◽  
Telomere Shortening ◽  
The Impact

Early-life environment is known to affect later-life health and disease, which could be mediated by the early-life programming of telomere length, a key hallmark of ageing. According to the fetal programming of telomere biology hypothesis, variation in prenatal exposure to hormones is likely to influence telomere length. Yet the contribution of key metabolic hormones, i.e. thyroid hormones (THs), has been largely ignored. We recently showed that in contrast to predictions, exposure to elevated prenatal THs increased postnatal telomere length in wild collared flycatchers, but the generality of such effect, its underlying proximate mechanisms and consequences on survival have not been investigated. We therefore conducted a comprehensive study evaluating the impact of THs on potential drivers of telomere dynamics (growth, post-natal THs, mitochondria and oxidative stress), telomere length and medium-term survival using wild great tits as a model system. While prenatal THs did not significantly affect telomere length after hatching (i.e. day 7), they influenced postnatal telomere shortening (i.e. shorter telomeres at day 14 and the following winter) but not apparent survival. Circulating THs, mitochondrial density or oxidative stress biomarkers were not significantly influenced, whereas TH-supplemented group showed accelerated growth, which may explain the observed delayed effect on telomeres. We discuss several alternative hypotheses that may explain the contrast with our previous findings in flycatchers. Given that shorter telomeres in early life tend to be carried until adulthood and are often associated with decreased survival prospects, the effects of prenatal THs on telomeres may have long-lasting effects on senescence.

Longer Telomere Length in Elite Master Sprinters: Relationship to Performance and Body Composition

2017 ◽  
Vol 38 (14) ◽  
pp. 1111-1116 ◽  
Author(s):  
Herbert Simoes ◽  
Caio Sousa ◽  
Thiago dos Santos Rosa ◽  
Samuel da Silva Aguiar ◽  
Lysleine Deus ◽  
...  
Keyword(s):  
Telomere Length ◽  
Body Fat ◽  
Healthy Lifestyle ◽  
Significant Negative Correlation ◽  
Performance Level ◽  
Master Athletes ◽  
Actual Performance ◽  
And Performance ◽  
Underlying Mechanisms ◽  
High Level

AbstractEmergent evidence suggests that the long-term healthy lifestyle of master athletes may attenuate aging. We compared telomere length (TL) of high-level master sprinters and non-athlete age-matched controls, and analyzed the relationships of TL with performance and body fat. Elite master sprinters (n=11; aged 50.1±9.2yrs) and healthy untrained controls (n=10; aged 45.4±10.9yrs) had blood samples collected for biochemical and biomolecular analyses. Master sprinters had longer TL, lower body fat and BMI, and a better lipid profile than age-matched controls (p<0.05). A large effect size was verified comparing TL between athletes vs. controls (Cohen’s d=1.039), with a significant negative correlation between TL and performance decline per decade (r=−0.624, p<0.01) and a positive correlation of TL and actual performance level (r=0.641, p<0.01). In conclusion, TL of elite master sprinters was longer than their untrained peers, and seems to be not only a marker of health status, but also an indicator of sports longevity since both actual performance level and its decrease over years were related to TL. Further research might assess the TL of elite master endurance athletes for comparison with sprinters, and also investigate the underlying mechanisms by which the attenuation of telomere shortening occurs in master athletes.

The Possible Role of Telomere Length and Chemokines in the Aging Process: A Transdiagnostic Review in Psychiatry

2019 ◽  
Vol 15 (3) ◽  
pp. 171-192
Author(s):  
Fernanda Endler Valiati ◽  
Gabriel Henrique Hizo ◽  
Jairo Vinícius Pinto ◽  
Márcia Kauer-Sant`Anna
Keyword(s):  
Psychiatric Disorders ◽  
Telomere Length ◽  
Aging Process ◽  
Accelerated Aging ◽  
Premature Death ◽  
Mental Illnesses ◽  
Telomere Shortening ◽  
Early Aging ◽  
The Relationship

Background: Psychiatric disorders are common, reaching a worldwide prevalence of 29.2%. They are associated with a high risk of premature death and with accelerated aging in clinical, molecular and neuroimaging studies. Recently, there is strong evidence suggesting a possible role of telomere length and chemokines in aging processes in psychiatric disorders. Objective: We aimed to review the literature on telomere length and chemokines and its association with early aging in mental illnesses on a transdiagnostic approach. Results: The review highlights the association between psychiatric disorders and early aging. Several independent studies have reported shorter telomere length and dysregulations on levels of circulating chemokines in schizophrenia, bipolar disorder, major depressive disorder, and anxiety disorders, suggesting a complex interaction between these markers in a transdiagnostic level. However, studies have investigated the inflammatory markers and telomere shortening separately and associated with a particular diagnosis, rather than as a transdiagnostic biological feature. Conclusion: There is consistent evidence supporting the relationship between accelerated aging, telomere length, and chemokines in mental disorders, but they have been studied individually. Thus, more research is needed to improve the knowledge of accelerated senescence and its biomarkers in psychiatry, not only individually in each diagnosis, but also based on a transdiagnostic perspective. Moreover, further research should try to elucidate how the intricate association between the chemokines and telomeres together may contribute to the aging process in psychiatric disorders.

scholarly journals Telomerase as a Therapeutic Target in Cardiovascular Disease

2021 ◽  
Vol 41 (3) ◽  
pp. 1047-1061
Author(s):  
Jedrzej Hoffmann ◽  
Gavin Richardson ◽  
Judith Haendeler ◽  
Joachim Altschmied ◽  
Vicente Andrés ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Reverse Transcriptase ◽  
Telomere Length ◽  
Therapeutic Target ◽  
Genetic Disorders ◽  
Telomerase Reverse Transcriptase ◽  
Loss Of Function ◽  
Antioxidative Function ◽  
Underlying Mechanisms ◽  
The Impact

Shortened telomeres have been linked to numerous chronic diseases, most importantly coronary artery disease, but the underlying mechanisms remain ill defined. Loss-of-function mutations and deletions in telomerase both accelerate telomere shortening but do not necessarily lead to a clinical phenotype associated with atherosclerosis, questioning the causal role of telomere length in cardiac pathology. The differential extranuclear functions of the 2 main components of telomerase, telomerase reverse transcriptase and telomerase RNA component, offer important clues about the complex relationship between telomere length and cardiovascular pathology. In this review, we critically discuss relevant preclinical models, genetic disorders, and clinical studies to elucidate the impact of telomerase in cardiovascular disease and its potential role as a therapeutic target. We suggest that the antioxidative function of mitochondrial telomerase reverse transcriptase might be atheroprotective, making it a potential target for clinical trials. Graphic Abstract: A graphic abstract is available for this article.

scholarly journals The integration of epigenetics and genetics in nutrition research for CVD risk factors

2016 ◽  
Vol 76 (3) ◽  
pp. 333-346 ◽  
Author(s):  
Yiyi Ma ◽  
Jose M. Ordovas
Keyword(s):  
Dna Methylation ◽  
Intervention Studies ◽  
Review Paper ◽  
Scientific Evidence ◽  
Current Evidence ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Nutrition Research ◽  
Underlying Mechanisms ◽  
High Level

There is increasing evidence documenting gene-by-environment (G × E) interactions for CVD related traits. However, the underlying mechanisms are still unclear. DNA methylation may represent one of such potential mechanisms. The objective of this review paper is to summarise the current evidence supporting the interplay among DNA methylation, genetic variants, and environmental factors, specifically (1) the association between SNP and DNA methylation; (2) the role that DNA methylation plays in G × E interactions. The current evidence supports the notion that genotype-dependent methylation may account, in part, for the mechanisms underlying observed G × E interactions in loci such asAPOE, IL6and ATP-binding cassette A1. However, these findings should be validated using intervention studies with high level of scientific evidence. The ultimate goal is to apply the knowledge and the technology generated by this research towards genetically based strategies for the development of personalised nutrition and medicine.

scholarly journals Trends in Natural Nutrients for Oxidative Stress and Cell Senescence

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Navid Omidifar ◽  
Mohsen moghadami ◽  
Seyyed Mojtaba Mousavi ◽  
Seyyed Alireza Hashemi ◽  
Ahmad Gholami ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Olive Oil ◽  
Disease Progression ◽  
Dietary Patterns ◽  
Aging Process ◽  
Cell Senescence ◽  
Telomere Shortening ◽  
Age Related ◽  
Dietary Components ◽  
Underlying Mechanisms

Due to the increase in the aged population and increased life expectancy, the underlying mechanisms involved in the aging process and cell senescence and the ways for modulating these processes in age-related diseases become important. One of the main mechanisms involved in aging and cell senescence, especially in the diseases related to aging, is the oxidative stress process and the following inflammation. Hence, the effects of antioxidants are highlighted in the literature due to their beneficial impacts on inhibiting telomere shortening or DNA damage and other processes related to aging and cell senescence in age-related diseases. Dietary components, foods, and dietary patterns rich in antioxidants can modulate the aging process and delay the progression of some chronic diseases such as cardiovascular diseases, diabetes, and Alzheimer’s disease. Foods high in polyphenols, vitamin C, or carotenoids, olive oil, seeds, nuts, legumes, dietary supplements such as CoQ10, and some other dietary factors are the most important nutritional sources that have high antioxidant contents which can positively affect cell senescence and disease progression. Plant dietary patterns including Mediterranean diets can also inhibit telomere shortening following oxidative damages, and this can delay cell aging and senescence in age-related diseases. Further, olive oil can inhibit protein aggregation in Alzheimer’s disease. It can be concluded that nutrition can delay the process of cell senescence in age-related diseases via inhibiting oxidative and inflammatory pathways. However, more studies are needed to better clarify the underlying mechanisms of nutrition and dietary components on cell senescence, aging, and disease progression, especially those related to age.

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