ArticleAntioxidants & redox signaling2012
The characterization of the Caenorhabditis elegans mitochondrial thioredoxin system uncovers an unexpected protective role of thioredoxin reductase 2 in β-amyloid peptide toxicity.
Article in Antioxidants & redox signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 52 citations in OpenAlex.
- Mitochondrial redox homeostasis links organellar stress surveillance to germline and somatic integrity in Caenorhabditis elegans.Redox biology · 2026Article
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- Evolutionarily Conserved Role of Thioredoxin Systems in Determining Longevity.Antioxidants (Basel, Switzerland) · 2023Review
- Mitochondrial thioredoxin system is required for enhanced stress resistance and extended longevity in long-lived mitochondrial mutants.Redox biology · 2022Article
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- Activation of mitochondrial unfolded protein response protects against multiple exogenous stressors.Life science alliance · 2021Article
- Vitamin BCell reports · 2021Article
- Mitochondrial hydrogen peroxide positively regulates neuropeptide secretion during diet-induced activation of the oxidative stress response.Nature communications · 2021Article
- Beneficial and Detrimental Effects of Reactive Oxygen Species on Lifespan: A Comprehensive Review of Comparative and Experimental Studies.Frontiers in cell and developmental biology · 2021Review
- Loss of glutathione redox homeostasis impairs proteostasis by inhibiting autophagy-dependent protein degradation.Cell death and differentiation · 2019Article
- Redox-dependent and redox-independent functions of Caenorhabditis elegans thioredoxin 1.Redox biology · 2019Article
- The glutathione system and the related thiol network in Caenorhabditis elegans.Redox biology · 2019Review
- Cytoplasmic and Mitochondrial NADPH-Coupled Redox Systems in the Regulation of Aging.Nutrients · 2019Review
- Cause or casualty: The role of mitochondrial DNA in aging and age-associated disease.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- The Architecture of Thiol Antioxidant Systems among Invertebrate Parasites.Molecules (Basel, Switzerland) · 2017Review
- Glutathione reductase gsr-1 is an essential gene required for Caenorhabditis elegans early embryonic development.Free radical biology & medicine · 2016Article
- TRX-1 Regulates SKN-1 Nuclear Localization Cell Non-autonomously in Caenorhabditis elegans.Genetics · 2016Article
- Omega-3 fatty acid obtained from Nannochloropsis oceanica cultures grown under low urea protect against Abeta-induced neural damage.Journal of food science and technology · 2015Article
- Comparative mapping of the 22q11.2 deletion region and the potential of simple model organisms.Journal of neurodevelopmental disorders · 2015Article
- Growth hormone alters the glutathione S-transferase and mitochondrial thioredoxin systems in long-living Ames dwarf mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2014Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimFunctional in vivo studies on the mitochondrial thioredoxin system are hampered by the embryonic or larval lethal phenotypes displayed by murine or Drosophila knock-out models. Thus, the access to alternative metazoan knock-out models for the mitochondrial thioredoxin system is of critical importance.
resultsWe report here the characterization of the mitochondrial thioredoxin system of Caenorhabditis elegans that is composed of the genes trx-2 and trxr-2. We demonstrate that the proteins thioredoxin 2 (TRX-2) and thioredoxin reductase 2 (TRXR-2) localize to the mitochondria of several cells and tissues of the nematode and that trx-2 and trxr-2 are upregulated upon induction of the mitochondrial unfolded protein response. Surprisingly, C. elegans trx-2 (lof ) and trxr-2 (null) single and double mutants are viable and display similar growth rates as wild-type controls. Moreover, the lack of the mitochondrial thioredoxin system does not affect longevity, reactive oxygen species production or the apoptotic program. Interestingly, we found a protective role of TRXR-2 in a transgenic nematode model of Alzheimer's disease (AD) that expresses human β-amyloid peptide and causes an age-dependent progressive paralysis. Hence, trxr-2 downregulation enhanced the paralysis phenotype, while a strong decrease of β-amyloid peptide and amyloid deposits occurred when TRXR-2 was overexpressed. INNOVATION: C. elegans provides the first viable metazoan knock-out model for the mitochondrial thioredoxin system and identifies a novel role of this system in β-amyloid peptide toxicity and AD.
conclusionThe nematode strains characterized in this work make C. elegans an ideal model organism to study the pathophysiology of the mitochondrial thioredoxin system at the level of a complete organism.
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