scholarly journals Telomere shortening in patients on long-term hemodialysis

2021 ◽  
Author(s):  
Yucheng Wang ◽  
Siyu Chen ◽  
Shi Feng ◽  
Cuili Wang ◽  
Hong Jiang ◽  
...  
Keyword(s):  
Telomere Shortening

scholarly journals Nestling telomere shortening, but not telomere length, reflects developmental stress and predicts survival in wild birds

2014 ◽  
Vol 281 (1785) ◽  
pp. 20133287 ◽  
Author(s):  
Jelle J. Boonekamp ◽  
G. A. Mulder ◽  
H. Martijn Salomons ◽  
Cor Dijkstra ◽  
Simon Verhulst
Keyword(s):  
Telomere Length ◽  
Brood Size ◽  
Developmental Stress ◽  
Free Living ◽  
Telomere Shortening ◽  
Developmental Effects ◽  
Fitness Consequences ◽  
Developmental Conditions ◽  
Fledgling Mass

Developmental stressors often have long-term fitness consequences, but linking offspring traits to fitness prospects has remained a challenge. Telomere length predicts mortality in adult birds, and may provide a link between developmental conditions and fitness prospects. Here, we examine the effects of manipulated brood size on growth, telomere dynamics and post-fledging survival in free-living jackdaws. Nestlings in enlarged broods achieved lower mass and lost 21% more telomere repeats relative to nestlings in reduced broods, showing that developmental stress accelerates telomere shortening. Adult telomere length was positively correlated with their telomere length as nestling ( r = 0.83). Thus, an advantage of long telomeres in nestlings is carried through to adulthood. Nestling telomere shortening predicted post-fledging survival and recruitment independent of manipulation and fledgling mass. This effect was strong, with a threefold difference in recruitment probability over the telomere shortening range. By contrast, absolute telomere length was neither affected by brood size manipulation nor related to survival. We conclude that telomere loss, but not absolute telomere length, links developmental conditions to subsequent survival and suggest that telomere shortening may provide a key to unravelling the physiological causes of developmental effects on fitness.

scholarly journals Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner

Blood ◽  
2014 ◽  
Vol 123 (20) ◽  
pp. 3105-3115 ◽  
Author(s):  
Lijian Shao ◽  
Wei Feng ◽  
Hongliang Li ◽  
David Gardner ◽  
Yi Luo ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Total Body Irradiation ◽  
Bone Marrow Suppression ◽  
Premature Senescence ◽  
Independent Manner ◽  
Telomere Shortening ◽  
Key Points ◽  
Total Body

Key Points Total body irradiation causes long-term bone marrow suppression by selectively inducing HSC senescence. The induction of HSC senescence is independent of telomere shortening and p16Ink4a and Arf.

scholarly journals Leukocyte telomere length in patients with multiple sclerosis and its association with clinical phenotypes

2020 ◽  
Author(s):  
Michael Hecker ◽  
Brit Fitzner ◽  
Kathrin Jäger ◽  
Jan Bühring ◽  
Margit Schwartz ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Biological Aging ◽  
Leukocyte Telomere Length ◽  
Telomere Shortening ◽  
Secondary Progressive ◽  
Relapsing Remitting ◽  
Age And Sex

AbstractAging is a significant factor influencing the course of multiple sclerosis (MS). Accelerated telomere attrition is an indicator of premature biological aging and a potential contributor to various chronic diseases, including neurological disorders. However, there is currently a lack of studies focusing on telomere lengths in patients with MS.We measured the average leukocyte telomere length (LTL) in biobanked DNA samples of 40 relapsing-remitting MS patients (RRMS), 20 primary progressive MS patients (PPMS) and 60 healthy controls using a multiplex quantitative polymerase chain reaction method. Changes in LTL over a period of >10 years were evaluated in a subset of 10 patients. Association analyses of baseline LTL with the long-term clinical profiles of the patients were performed using inferential statistical tests and regression models adjusted for age and sex.The cross-sectional analysis revealed that the RRMS group was characterized by a significantly shorter relative LTL, on average, as compared to the PPMS group and controls. Shorter telomeres at baseline were also associated with a higher conversion rate from RRMS to secondary progressive MS (SPMS) in the 10-year follow-up. The LTL decrease over time was similar in RRMS patients and PPMS patients in the longitudinal analysis.Our data suggest a possible contributory role of accelerated telomere shortening in the pathobiology of MS. The interplay between disease-related immune system alterations, immunosenescence and telomere dynamics deserves further investigation. New insights into the mechanisms of disease might be obtained, e.g., by exploring the distribution of telomere lengths in specific blood cell populations.Research in contextEvidence before this studyThere is a growing research interest in the relationship between age and the pathophysiology and clinical presentation of multiple sclerosis (MS). Telomere shortening is a hallmark of biological aging. However, the role of telomeres in this chronic immune-mediated neurodegenerative disease has not yet been widely studied. Two research groups provided evidence that the telomeres of immune cells in the peripheral blood are shorter in patients with MS than in healthy subjects.Added value of this studyWe found that leukocytes from patients with relapsing-remitting MS (RRMS) are characterized by relatively short telomere lengths (TL). On average, we observed 18% shorter TL in the RRMS patient cohort (n=40) than in the age- and sex-matched healthy control cohort (n=60). We further analyzed the association of TL and long-term clinical outcomes. RRMS patients with shorter TL had a higher rate of converting to secondary progressive MS over a 10-year follow-up period.Implications of all the available evidenceAs we and others have shown, TL are generally shorter in MS patients and associated with disease progression, independent of age. These findings suggest a link between biological aging and the heterogeneous clinical course of MS patients. It currently remains unclear whether shortened telomeres in MS are a cause or a consequence of the pathophysiological processes. Further studies with larger patient cohorts and different cell populations will be needed to expand our knowledge of age-related disease mechanisms and the use of TL as a biomarker in MS.

scholarly journals The effect of long-term ultra-endurance exercise and SOD2 genotype on telomere shortening with age

2020 ◽  
Vol 129 (4) ◽  
pp. 873-879 ◽  
Author(s):  
Barbara Hernando ◽  
Marta Gil-Barrachina ◽  
Elena Tomás-Bort ◽  
Ignacio Martinez-Navarro ◽  
Eladio Collado-Boira ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Endurance Training ◽  
Telomere Length ◽  
Endurance Exercise ◽  
Biological Aging ◽  
Acute Inflammatory Response ◽  
Telomere Shortening ◽  
Ultra Endurance ◽  
First Time

Habitual ultra-endurance exercise seems to promote telomere length maintenance, especially at older ages. In addition, the beneficial effect of ultra-endurance training on biological aging is higher in ultra-trail runners who have been engaged to ultra-endurance training during many years. Finally, and for the first time, this study shows that the SOD2 rs4880 polymorphism has a significant impact on telomere length, as well as on acute inflammatory response to a 107-km trail race.

Dynamics of telomeric chromatin at the crossroads of aging and cancer

2010 ◽  
Vol 48 ◽  
pp. 147-164 ◽  
Author(s):  
Jing Ye ◽  
Yunlin Wu ◽  
Eric Gilson
Keyword(s):  
Chromosomal Instability ◽  
Cellular Proliferation ◽  
Human Cancer ◽  
Chromosome Instability ◽  
Telomere Dysfunction ◽  
Promising Candidate ◽  
Telomere Shortening ◽  
Anti Cancer ◽  
Protein Components

Telomeres are nucleoprotein structures that protect the ends of human chromosomes through the formation of a ‘cap’, thus preventing exonucleolytic degradation, inter- and intra-chromosomal fusion, and subsequent chromosomal instability. During aging, telomere shortening correlates with tissue dysfunction and loss of renewal capacity. In human cancer, telomere dysfunction is involved in early chromosome instability, long-term cellular proliferation, and possibly other processes related to cell survival and microenvironment. Telomeres constitute an attractive target for the development of novel small-molecule anti-cancer drugs. In particular, individual protein components of the core telomere higher-order chromatin structure (known as the telosome or ‘shelterin’ complex) are promising candidate targets for cancer therapy.

scholarly journals Replicative senescence dictates the emergence of disease-associated microglia and contributes to Aβ pathology

2021 ◽  
Author(s):  
Yanling Hu ◽  
Gemma L. Fryatt ◽  
Mohammadmersad Ghorbani ◽  
Juliane Obst ◽  
David A. Menassa ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Replicative Senescence ◽  
Post Mortem ◽  
Telomere Shortening ◽  
Transcriptional Signature ◽  
Microglial Proliferation ◽  
Long Term Impact ◽  
Repeated Cycling

ABSTRACTThe sustained proliferation of microglia is a key hallmark of Alzheimer’s disease (AD), accelerating its progression. Here, we sought to understand the long-term impact of the early and prolonged microglial proliferation observed in AD, hypothesising that extensive and repeated cycling would engender a distinct transcriptional and phenotypic trajectory. We found that the early and sustained microglial proliferation seen in an AD-like model promotes replicative senescence, characterised by increased βgal activity, a senescence-associated transcriptional signature and telomere shortening, correlating with the appearance of disease-associated microglia (DAM) and senescent microglial profiles in human post-mortem AD cases. Prevention of early microglial proliferation hindered the development of senescence and DAM, impairing the accumulation of Aβ and associated neuritic damage. Overall, our results support that excessive microglial proliferation leads to the generation of senescent DAM, which contribute to early Aβ pathology in AD.

Sign in / Sign up

Export Citation Format

Share Document