ArticleBMC systems biology2014
Stress induced telomere shortening: longer life with less mutations?
Article in BMC systems biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Physiological mechanisms of adaptive developmental plasticity in Rana temporaria island populations.BMC evolutionary biology · 2017Article
- Mechanisms of DNA damage, repair, and mutagenesis.Environmental and molecular mutagenesis · 2017Review
- Corticosterone, inflammation, immune status and telomere length in frigatebird nestlings facing a severe herpesvirus infection.Conservation physiology · 2017Article
- Expression of Telomere Repeat Binding Factor 1 and TRF2 in Prostate Cancer and Correlation with Clinical Parameters.BioMed research international · 2017Article
- Interaction between Obstructive Sleep Apnea and Shortened Telomere Length on Brain White Matter Abnormality.Sleep · 2016Observational
- Quantifying replicative senescence as a tumor suppressor pathway and a target for cancer therapy.Scientific reports · 2015Article
- Review
- Telomeric aging: mitotic clock or stress indicator?Frontiers in genetics · 2015Article
- GHK and DNA: resetting the human genome to health.BioMed research international · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMutations accumulate as a result of DNA damage and imperfect DNA repair machinery. In higher eukaryotes the accumulation and spread of mutations is limited in two primary ways: through p53-mediated programmed cell death and cellular senescence mediated by telomeres. Telomeres shorten at every cell division and cell stops dividing once the shortest telomere reaches a critical length. It has been shown that the rate of telomere attrition is accelerated when cells are exposed to DNA damaging agents. However the implications of this mechanism are not fully understood.
resultsWith the help of in silico model we investigate the effect of genotoxic stress on telomere attrition and apoptosis in a population of non-identical replicating cells. When comparing the populations of cells with constant vs. stress-induced rate of telomere shortening we find that stress induced telomere shortening (SITS) increases longevity while reducing mutation rate. Interestingly, however, the effect takes place only when genotoxic stresses (e.g. reactive oxygen species due to metabolic activity) are distributed non-equally among cells.
conclusionsOur results for the first time show how non-equal distribution of metabolic load (and associated genotoxic stresses) combined with stress induced telomere shortening can delay aging and minimize mutations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.