ArticlePLoS genetics2015
Mitochondrial and cytoplasmic ROS have opposing effects on lifespan.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
What it found
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Who cites it
125 citing papers in PubMed, 207 citations in OpenAlex.
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- Respirometry-Based Screening of Marine Natural Products Identifies Leptochelin A as a Novel Modulator of Mitochondrial Function.Oxidative medicine and cellular longevity · 2026Article
- Iron-deplete diet enhances Caenorhabditis elegans lifespan via oxidative stress response pathways.The EMBO journal · 2025Article
- A gut-brain-gut axis orchestrates host responses counteracting microbiome-induced iron insufficiency.The EMBO journal · 2025Article
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- Iron-deplete diet enhancesbioRxiv : the preprint server for biology · 2025Article
- Developmental disruption of the mitochondrial fission gene drp-1 extends the longevity of daf-2 insulin/IGF-1 receptor mutant.GeroScience · 2025Article
- Lifespan Extension and Motor Function Improvement Effects of Whale Meat Extract inInternational journal of molecular sciences · 2024Article
- Inflammaging and Brain Aging.International journal of molecular sciences · 2024Review
- Exploring the Role of Reactive Oxygen Species in the Pathogenesis and Pathophysiology of Alzheimer's and Parkinson's Disease and the Efficacy of Antioxidant Treatment.Antioxidants (Basel, Switzerland) · 2024Review
- NEKL-4 regulates microtubule stability and mitochondrial health in ciliated neurons.The Journal of cell biology · 2024Article
- Mitochondrial Dysfunctions: Genetic and Cellular Implications Revealed by Various Model Organisms.Genes · 2024Review
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- Socialized mitochondria: mitonuclear crosstalk in stress.Experimental & molecular medicine · 2024Review
- Redox regulation in lifespan determination.The Journal of biological chemistry · 2024Review
- Mitochondrial recovery by the UPRSeminars in cell & developmental biology · 2024Review
65 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
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Reactive oxygen species (ROS) are highly reactive, oxygen-containing molecules that can cause molecular damage within the cell. While the accumulation of ROS-mediated damage is widely believed to be one of the main causes of aging, ROS also act in signaling pathways. Recent work has demonstrated that increasing levels of superoxide, one form of ROS, through treatment with paraquat, results in increased lifespan. Interestingly, treatment with paraquat robustly increases the already long lifespan of the clk-1 mitochondrial mutant, but not other long-lived mitochondrial mutants such as isp-1 or nuo-6. To genetically dissect the subcellular compartment in which elevated ROS act to increase lifespan, we deleted individual superoxide dismutase (sod) genes in clk-1 mutants, which are sensitized to ROS. We find that only deletion of the primary mitochondrial sod gene, sod-2 results in increased lifespan in clk-1 worms. In contrast, deletion of either of the two cytoplasmic sod genes, sod-1 or sod-5, significantly decreases the lifespan of clk-1 worms. Further, we show that increasing mitochondrial superoxide levels through deletion of sod-2 or treatment with paraquat can still increase lifespan in clk-1;sod-1 double mutants, which live shorter than clk-1 worms. The fact that mitochondrial superoxide can increase lifespan in worms with a detrimental level of cytoplasmic superoxide demonstrates that ROS have a compartment specific effect on lifespan - elevated ROS in the mitochondria acts to increase lifespan, while elevated ROS in the cytoplasm decreases lifespan. This work also suggests that both ROS-dependent and ROS-independent mechanisms contribute to the longevity of clk-1 worms.
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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.