ArticleAging cell2015
A peroxiredoxin, PRDX-2, is required for insulin secretion and insulin/IIS-dependent regulation of stress resistance and longevity.
Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 68 citations in OpenAlex.
- Peroxiredoxin 1 safeguards the nucleolar genome from oxidative damage.Science advances · 2026Article
- Fasting requires Peroxiredoxin 2 and Peroxiredoxin 6 to coordinate redox dependent mitochondrial and lipid remodelling in Caenorhabditis elegans.Redox biology · 2026Article
- Exercise-related microRNAs in Caenorhabditis elegans regulate calcium homeostasis and mitochondrial dynamics: Conserved pathways, divergent microRNAs.The FEBS journal · 2026Article
- Article
- Amitriptyline increases food intake via prdx-2 without altering other physiological parameters in C. elegans under a modified bacterial diet.Scientific reports · 2025Article
- Full-length direct RNA sequencing reveals extensive remodeling of RNA expression, processing and modification in aging Caenorhabditis elegans.Nucleic acids research · 2024Article
- Article
- Neuronal PRDX-2-Mediated ROS Signaling Regulates Food Digestion via peripheral UPRNature communications · 2024Article
- Endogenous hydrogen peroxide positively regulates secretion of a gut-derived peptide in neuroendocrine potentiation of the oxidative stress response inbioRxiv : the preprint server for biology · 2024Article
- Full-length direct RNA sequencing reveals extensive remodeling of RNA expression, processing and modification in agingbioRxiv : the preprint server for biology · 2024Article
- Peroxiredoxin 2 is required for the redox mediated adaptation to exercise.Redox biology · 2023Article
- Hydrogen peroxide detoxification through the peroxiredoxin/thioredoxin antioxidant system: A look at the pancreatic β-cell oxidant defense.Vitamins and hormones · 2023Article
- Integrative single-cell RNA and ATAC sequencing reveals that the FOXO1-PRDX2-TNF axis regulates tendinopathy.Frontiers in immunology · 2023Article
- PMFrontiers in public health · 2023Article
- Exploiting Polyphenol-Mediated Redox Reorientation in Cancer Therapy.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Oxidation and Antioxidation of Natural Products in the Model OrganismAntioxidants (Basel, Switzerland) · 2022Review
- The Intestinal Redox System and Its Significance in Chemotherapy-Induced Intestinal Mucositis.Oxidative medicine and cellular longevity · 2022Review
- Metabolic and behavioral effects of olanzapine and fluoxetine on the model organismSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021Article
- The Role of Thioredoxin/Peroxiredoxin in the β-Cell Defense Against Oxidative Damage.Frontiers in endocrinology · 2021Review
- A Complex Proteomic Response of the Parasitic Nematode Anisakis simplex s.s. to Escherichia coliLipopolysaccharide.Molecular & cellular proteomics : MCP · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Peroxiredoxins (Prx) are abundant thiol peroxidases with a conserved anti-ageing role. In contrast to most animals, the nematode worm, Caenorhabditis elegans, encodes a single cytosolic 2-Cys Prx, PRDX-2, rendering it an excellent model for examining how peroxiredoxins affect animal physiology and ageing. Our previous work revealed that, although PRDX-2 protects against the toxicity of peroxides, enigmatically, prdx-2-mutant animals are hyper-resistant to other forms of oxidative stress. Here, we have investigated the basis for this increased resistance. Mammalian FOXO and Nrf2 transcription factors directly promote the expression of a range of detoxification enzymes. We show that the FOXO orthologue, DAF-16, and the Nrf2 orthologue, SKN-1, are required for the increased stress resistance of prdx-2-mutant worms. Our data suggest that PRDX-2 is required for normal levels of insulin secretion and hence the inhibition of DAF-16 and SKN-1 by insulin/IGF-1-like signalling (IIS) under nutrient-rich conditions. Intriguingly, loss of PRDX-2 increases DAF-16 and SKN-1 activities sufficiently to increase arsenite resistance without initiating other IIS-inhibited processes. Together, these data suggest that loss of peroxiredoxin function may increase stress resistance by reducing insulin secretion, but that further changes in insulin signalling are required for the reprogramming of development and fat metabolism. In addition, we reveal that the temperature-dependent prolongevity function of PRDX-2 is required for the extended lifespan associated with several pathways, including further reductions in IIS.
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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.