ArticleRedox biology2022
Mitochondrial thioredoxin system is required for enhanced stress resistance and extended longevity in long-lived mitochondrial mutants.
Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Thioredoxin reductase-1 facilitates cellular plasticity and stemness mediated by TGF-β1 in non-small cell lung cancer.Cancer biology & therapy · 2026Article
- Elevated mitochondrial superoxide promotes longevity through a mitochondria-to-nucleus kinase signaling pathway.Redox biology · 2026Article
- Article
- 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
- 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
- A mitochondria-targeted aggregation-induced emission photosensitizer for eradicationSmart molecules : open access · 2025Article
- Developmental disruption of the mitochondrial fission gene drp-1 extends the longevity of daf-2 insulin/IGF-1 receptor mutant.GeroScience · 2025Article
- Thioredoxin System in Insects: Uncovering the Roles of Thioredoxins and Thioredoxin Reductase beyond the Antioxidant Defences.Insects · 2024Review
- Overexpression of mitochondrial fission or mitochondrial fusion genes enhances resilience and extends longevity.Aging cell · 2024Article
- Navigating the Landscape of Translational Geroscience in Canada: A Comprehensive Evaluation of Current Progress and Future Directions.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- Thioredoxin (Trx): A redox target and modulator of cellular senescence and aging-related diseases.Redox biology · 2024Review
- Synchronization by bleaching does not affect longevity.microPublication biology · 2024Article
- RNA Sequencing of Pooled Samples Effectively Identifies Differentially Expressed Genes.Biology · 2023Article
- Evolutionarily Conserved Role of Thioredoxin Systems in Determining Longevity.Antioxidants (Basel, Switzerland) · 2023Review
- Endosomal trafficking protein TBC-2 is required for the longevity of long-lived mitochondrial mutants.Frontiers in aging · 2023Article
- Selenoproteins and the senescence-associated epitranscriptome.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- S-Denitrosylation: A Crosstalk between Glutathione and Redoxin Systems.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Mild impairment of mitochondrial function has been shown to increase lifespan in genetic model organisms including worms, flies and mice. To better understand the mechanisms involved, we analyzed RNA sequencing data and found that genes involved in the mitochondrial thioredoxin system, trx-2 and trxr-2, are specifically upregulated in long-lived mitochondrial mutants but not other non-mitochondrial, long-lived mutants. Upregulation of trx-2 and trxr-2 is mediated by activation of the mitochondrial unfolded protein response (mitoUPR). While we decided to focus on the genes of the mitochondrial thioredoxin system for this paper, we identified multiple other antioxidant genes that are upregulated by the mitoUPR in the long-lived mitochondrial mutants including sod-3, prdx-3, gpx-6, gpx-7, gpx-8 and glrx-5. In exploring the role of the mitochondrial thioredoxin system in the long-lived mitochondrial mutants, nuo-6 and isp-1, we found that disruption of either trx-2 or trxr-2 significantly decreases their long lifespan, but has no effect on wild-type lifespan, indicating that the mitochondrial thioredoxin system is specifically required for their longevity. In contrast, disruption of the cytoplasmic thioredoxin gene trx-1 decreases lifespan in nuo-6, isp-1 and wild-type worms, indicating a non-specific detrimental effect on longevity. Disruption of trx-2 or trxr-2 also decreases the enhanced resistance to stress in nuo-6 and isp-1 worms, indicating a role for the mitochondrial thioredoxin system in protecting against exogenous stressors. Overall, this work demonstrates an important role for the mitochondrial thioredoxin system in both stress resistance and lifespan resulting from mild impairment of mitochondrial function.
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Registered trials
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