ArticleCell2015
Early telomerase inactivation accelerates aging independently of telomere length.
Article in Cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
63 citing papers in PubMed, 123 citations in OpenAlex.
- Trial
- Differential effects of endurance, interval, and resistance training on telomerase activity and telomere length in a randomized, controlled study.European heart journal · 2019Trial
- Both genome instability and replicative senescence stem from the shortest telomere in telomerase-negative cells.Nature communications · 2026Article
- Nuclear actin and DNA replication stress regulate telomere maintenance by telomerase.Nature communications · 2025Article
- Mice carrying the homologous human shelterin POT1-L259S mutation linked to pulmonary fibrosis show a telomerase deficiency-like phenotype with telomere shortening with increasing mouse generations.Genes & development · 2025Article
- A COMPREHENSIVE CATALOG OF TELOMERE CONTENT VARIATION ACROSS HUMAN POPULATIONS.bioRxiv : the preprint server for biology · 2025Article
- Tissue Fibrosis Decoded via Cellular Senescence: Mechanisms, Treatments, and Emerging Technologies.Aging and disease · 2025Review
- NK Cell Senescence in Cancer: From Molecular Mechanisms to Therapeutic Opportunities.Aging and disease · 2025Review
- Mathematical model linking telomeres to senescence in Saccharomyces cerevisiae reveals cell lineage versus population dynamics.Nature communications · 2025Article
- Role of telomere dysfunction and immune infiltration in idiopathic pulmonary fibrosis: new insights from bioinformatics analysis.Frontiers in genetics · 2024Article
- Telomere maintenance and the DNA damage response: a paradoxical alliance.Frontiers in cell and developmental biology · 2024Article
- Involvement of Inheritance in Determining Telomere Length beyond Environmental and Lifestyle Factors.Aging and disease · 2023Review
- Article
- Challenges of COPD Patients during the COVID-19 Pandemic.Pathogens (Basel, Switzerland) · 2022Review
- Mad3 modulates the GScience advances · 2022Article
- Review
- Oridonin Delays Aging Through the AKT Signaling Pathway.Frontiers in pharmacology · 2022Article
- Telomere shortening causes distinct cell division regimes during replicative senescence in Saccharomyces cerevisiae.Cell & bioscience · 2021Article
- Inflammation, epigenetics, and metabolism converge to cell senescence and ageing: the regulation and intervention.Signal transduction and targeted therapy · 2021Review
- Is There an Interconnection between Epithelial-Mesenchymal Transition (EMT) and Telomere Shortening in Aging?International journal of molecular sciences · 2021Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Telomerase is required for long-term telomere maintenance and protection. Using single budding yeast mother cell analyses we found that, even early after telomerase inactivation (ETI), yeast mother cells show transient DNA damage response (DDR) episodes, stochastically altered cell-cycle dynamics, and accelerated mother cell aging. The acceleration of ETI mother cell aging was not explained by increased reactive oxygen species (ROS), Sir protein perturbation, or deprotected telomeres. ETI phenotypes occurred well before the population senescence caused late after telomerase inactivation (LTI). They were morphologically distinct from LTI senescence, were genetically uncoupled from telomere length, and were rescued by elevating dNTP pools. Our combined genetic and single-cell analyses show that, well before critical telomere shortening, telomerase is continuously required to respond to transient DNA replication stress in mother cells and that a lack of telomerase accelerates otherwise normal aging.
Indexed as
Identifiers
What OpenQuestion holds
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.