ArticleCell metabolism2013
Epigenetic silencing mediates mitochondria stress-induced longevity.
Article in Cell metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 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.
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Who cites it
119 citing papers in PubMed.
- Mitochondrial superoxide-induced mitohormesis is mediated by citrate and cardioprotective.Science advances · 2026Article
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- Tissue Fibrosis Decoded via Cellular Senescence: Mechanisms, Treatments, and Emerging Technologies.Aging and disease · 2025Review
- The advances in acetylation modification in senescence and aging-related diseases.Frontiers in physiology · 2025Review
- Interplay between epigenetics, senescence and cellular redox metabolism in cancer and its therapeutic implications.Redox biology · 2024Review
- Lithocholic Acid's Ionic Compounds as Promising Antitumor Agents: Synthesis and Evaluation of the Production of Reactive Oxygen Species (ROS) in Mitochondria.Antioxidants (Basel, Switzerland) · 2024Article
- Manipulating mitochondrial reactive oxygen species alters survival in unexpected ways in a Drosophila Cdk5 model of neurodegeneration.Biology open · 2024Article
- MANIPULATING MITOCHONDRIAL REACTIVE OXYGEN SPECIES ALTERS SURVIVAL IN UNEXPECTED WAYS IN AbioRxiv : the preprint server for biology · 2024Article
- Redox regulation in lifespan determination.The Journal of biological chemistry · 2024Review
- Potential Effects of Traditional Chinese Medicine in Anti-Aging and Aging-Related Diseases: Current Evidence and Perspectives.Clinical interventions in aging · 2024Review
- TheAging · 2023Article
- Yeast Chromatin Mutants Reveal Altered mtDNA Copy Number and Impaired Mitochondrial Membrane Potential.Journal of fungi (Basel, Switzerland) · 2023Article
- Targeting Mitochondria to Control Ageing and Senescence.Pharmaceutics · 2023Review
- Stimulation of RAS-dependent ROS signaling extends longevity by modulating a developmental program of global gene expression.Science advances · 2022Article
- Review
- Article
- Pleiotropic effects of mitochondria in aging.Nature aging · 2022Review
- Cellular functions of the protein kinase ATM and their relevance to human disease.Nature reviews. Molecular cell biology · 2021Review
- Shaping longevity early in life: developmental ROS and H3K4me3 set the clock.Cell cycle (Georgetown, Tex.) · 2021Article
- Empowering Melatonin Therapeutics withDiseases (Basel, Switzerland) · 2021Review
59 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors.
Funding
Abstract
Reactive oxygen species (ROS) play complex roles in aging, having both damaging effects and signaling functions. Transiently elevating mitochondrial stress, including mitochondrial ROS (mtROS), elicits beneficial responses that extend lifespan. However, these adaptive, longevity-signaling pathways remain poorly understood. We show here that Tel1p and Rad53p, homologs of the mammalian DNA damage response kinases ATM and Chk2, mediate a hormetic mtROS longevity signal that extends yeast chronological lifespan. This pathway senses mtROS in a manner distinct from the nuclear DNA damage response and ultimately imparts longevity by inactivating the histone demethylase Rph1p specifically at subtelomeric heterochromatin, enhancing binding of the silencing protein Sir3p, and repressing subtelomeric transcription. These results demonstrate the existence of conserved mitochondria-to-nucleus stress-signaling pathways that regulate aging through epigenetic modulation of nuclear gene expression.
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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.