ArticlePLoS biology2011
The homeobox protein CEH-23 mediates prolonged longevity in response to impaired mitochondrial electron transport chain in C. elegans.
Article in PLoS biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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Who cites it
58 citing papers in PubMed.
- Mitochondrial stress activates ELT-2-dependent lysosomal proteostasis to extend lifespan inScience advances · 2026Article
- MAK-2 Kinase Is Required for Extended Longevity and Enhanced Stress Resistance Resulting From Mild Impairment of Mitochondrial Function in isp-1 Mutants.Aging cell · 2026Article
- Mild Mitochondrial Impairment Activates Overlapping Longevity Pathways Converging on the Flavin-Containing Monooxygenase FMO-2.bioRxiv : the preprint server for biology · 2026Article
- Mild mitochondrial impairment activates overlapping longevity pathways converging on the flavin-containing monooxygenase FMO-2.Frontiers in aging · 2026Article
- The homeodomain transcription factor CEH-37 regulates PMK-1/p38 MAPK pathway to protect against intestinal infection via the phosphatase VHP-1.Cellular and molecular life sciences : CMLS · 2023Article
- Article
- Endosomal trafficking protein TBC-2 modulates stress resistance and lifespan through DAF-16-dependent and independent mechanisms.Aging cell · 2023Article
- Endosomal trafficking protein TBC-2 is required for the longevity of long-lived mitochondrial mutants.Frontiers in aging · 2023Article
- Mitochondrial protein import determines lifespan through metabolic reprogramming and de novo serine biosynthesis.Nature communications · 2022Article
- Hijacking Cellular Stress Responses to Promote Lifespan.Frontiers in aging · 2022Review
- Mild mitochondrial impairment enhances innate immunity and longevity through ATFS-1 and p38 signaling.EMBO reports · 2021Article
- MON-2, a Golgi protein, mediates autophagy-dependent longevity inScience advances · 2021Article
- Emerging topics in C. elegans aging research: Transcriptional regulation, stress response and epigenetics.Mechanisms of ageing and development · 2019Review
- Mitochondrial Oxidative Stress Impairs Energy Metabolism and Reduces Stress Resistance and Longevity ofOxidative medicine and cellular longevity · 2019Article
- BRCA1 and BARD1 mediate apoptotic resistance but not longevity upon mitochondrial stress inEMBO reports · 2018Article
- Adaptive homeostasis and the free radical theory of ageing.Free radical biology & medicine · 2018Review
- Functional Characterization of Novel Circular RNA Molecule, circzip-2 and Its Synthesizing Gene zip-2 in C. elegans Model of Parkinson's Disease.Molecular neurobiology · 2018Article
- Activation of DAF-16/FOXO by reactive oxygen species contributes to longevity in long-lived mitochondrial mutants in Caenorhabditis elegans.PLoS genetics · 2018Article
- Mitochondrial Stress Restores the Heat Shock Response and Prevents Proteostasis Collapse during Aging.Cell reports · 2017Article
- The mitochondrial unfolded protein response: Signaling from the powerhouse.The Journal of biological chemistry · 2017Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Recent findings indicate that perturbations of the mitochondrial electron transport chain (METC) can cause extended longevity in evolutionarily diverse organisms. To uncover the molecular basis of how altered METC increases lifespan in C. elegans, we performed an RNAi screen and revealed that three predicted transcription factors are specifically required for the extended longevity of mitochondrial mutants. In particular, we demonstrated that the nuclear homeobox protein CEH-23 uniquely mediates the longevity but not the slow development, reduced brood size, or resistance to oxidative stress associated with mitochondrial mutations. Furthermore, we showed that ceh-23 expression levels are responsive to altered METC, and enforced overexpression of ceh-23 is sufficient to extend lifespan in wild-type background. Our data point to mitochondria-to-nucleus communications to be key for longevity determination and highlight CEH-23 as a novel longevity factor capable of responding to mitochondrial perturbations. These findings provide a new paradigm for how mitochondria impact aging and age-dependent diseases.
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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.