ArticleCell2016
Mitochondrial Stress Induces Chromatin Reorganization to Promote Longevity and UPR(mt).
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 246 papers, 2 of them syntheses that pooled it.
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
246 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The Intersection of Mitophagy and Autism Spectrum Disorder: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Stress and circulating cell-free mitochondrial DNA: A systematic review of human studies, physiological considerations, and technical recommendations.Mitochondrion · 2021Pooled it
- Regulation of cellular proteostasis via mitochondrial protein import.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Form and function of actin impacts actin health and aging.iScience · 2026Article
- DVE-1 is a telomere-binding protein and links the NuRD complex to telomere regulation iniScience · 2026Article
- Discovery and preclinical validation of a translationally optimized mitochondrial complex I modulator for Alzheimer's disease.npj drug discovery · 2026Article
- A multilayered stress-response circuit: The mammalian mitochondrial UPR.The FEBS journal · 2026Review
- Metabolites with a message: impacts on epigenetics and implications for epimetabopathies.EMBO reports · 2026Review
- Mitochondrial stress activates ELT-2-dependent lysosomal proteostasis to extend lifespan inScience advances · 2026Article
- Mitochondrial quality control in health and disease: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Review
- FUBL-3/FUBP1 mediates mitochondrial stress-induced chromatin remodeling and longevity.Science advances · 2026Article
- Bacteria-derived glutarate mitigates Alzheimer's disease model pathology through autophagy-lysosomal pathway.Cell communication and signaling : CCS · 2026Article
- A Forward Genetic Screen inbioRxiv : the preprint server for biology · 2026Article
- Mitochondrial Enzymes Mimetic Ultrasmall Palladium Nanozymes Prevent Senescence and Neurodegeneration Through Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A Stress-Responsive Nuclear Factor, GLDI-8, Mediates Mitochondrial Stress Responses to ETC Dysfunction.International journal of molecular sciences · 2026Article
- Interplay between proteostasis pathways and innate immune responses inInfection and immunity · 2026Review
- Organellar insights in ageing and longevity.Nature cell biology · 2026Review
- Remembrance of things past: Towards a life-course biology of aging.PLoS biology · 2026Article
- Discovery and Preclinical Validation of a Clinically Optimized Mitochondrial Complex I Modulator for Alzheimer's Disease.bioRxiv : the preprint server for biology · 2026Article
186 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors.
Funding
Abstract
Organisms respond to mitochondrial stress through the upregulation of an array of protective genes, often perpetuating an early response to metabolic dysfunction across a lifetime. We find that mitochondrial stress causes widespread changes in chromatin structure through histone H3K9 di-methylation marks traditionally associated with gene silencing. Mitochondrial stress response activation requires the di-methylation of histone H3K9 through the activity of the histone methyltransferase met-2 and the nuclear co-factor lin-65. While globally the chromatin becomes silenced by these marks, remaining portions of the chromatin open up, at which point the binding of canonical stress responsive factors such as DVE-1 occurs. Thus, a metabolic stress response is established and propagated into adulthood of animals through specific epigenetic modifications that allow for selective gene expression and lifespan extension.
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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.