ArticleCell2014
The intrinsic apoptosis pathway mediates the pro-longevity response to mitochondrial ROS in C. elegans.
Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 195 papers.
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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.
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Who cites it
195 citing papers in PubMed, 359 citations in OpenAlex.
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- Multiple Molecular Pathways to Longevity: Opposing Gene Expression Programs Define Distinct Aging Strategies.bioRxiv : the preprint server for biology · 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
- Iron-deplete diet enhances Caenorhabditis elegans lifespan via oxidative stress response pathways.The EMBO journal · 2025Article
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- Mitochondrial Reactive Oxygen Species in Infection and Immunity.Biomolecules · 2024Review
- Redox regulation in lifespan determination.The Journal of biological chemistry · 2024Review
- Decreased ATF5 level contributes to improved mitochondrial function in oocytes exposed to vitrification stress.Frontiers in cell and developmental biology · 2024Article
- N-acetylcysteine may improve endometrial receptivity by modulating endometrial stromal cells in goats.Archives animal breeding · 2024Article
- A bacterial pathogen induces developmental slowing by high reactive oxygen species and mitochondrial dysfunction in Caenorhabditis elegans.Cell reports · 2023Article
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- Antimicrobial mitochondrial reactive oxygen species induction by lung epithelial immunometabolic modulation.PLoS pathogens · 2023Article
- RNA Sequencing of Pooled Samples Effectively Identifies Differentially Expressed Genes.Biology · 2023Article
- Mitochondrial Oxidative Metabolism: An Emerging Therapeutic Target to Improve CKD Outcomes.Biomedicines · 2023Review
135 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The increased longevity of the C. elegans electron transport chain mutants isp-1 and nuo-6 is mediated by mitochondrial ROS (mtROS) signaling. Here we show that the mtROS signal is relayed by the conserved, mitochondria-associated, intrinsic apoptosis signaling pathway (CED-9/Bcl2, CED-4/Apaf1, and CED-3/Casp9) triggered by CED-13, an alternative BH3-only protein. Activation of the pathway by an elevation of mtROS does not affect apoptosis but protects from the consequences of mitochondrial dysfunction by triggering a unique pattern of gene expression that modulates stress sensitivity and promotes survival. In vertebrates, mtROS induce apoptosis through the intrinsic pathway to protect from severely damaged cells. Our observations in nematodes demonstrate that sensing of mtROS by the apoptotic pathway can, independently of apoptosis, elicit protective mechanisms that keep the organism alive under stressful conditions. This results in extended longevity when mtROS generation is inappropriately elevated. These findings clarify the relationships between mitochondria, ROS, apoptosis, and aging.
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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.