ArticleThe EMBO journal2025
Iron-deplete diet enhances Caenorhabditis elegans lifespan via oxidative stress response pathways.
Article in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Aging regulation by gut microbiota: molecular insights from Caenorhabditis elegans.Biogerontology · 2026Review
- A Forward Genetic Screen inbioRxiv : the preprint server for biology · 2026Article
- RNA methyltransferase CMTR-1 inhibition activates a GATA transcription factor-mediated protective immune response.PLoS pathogens · 2026Article
- Iron overload disrupts lipid desaturation through SKN-1 signaling inMaterials today. Bio · 2026Article
- Cycloastragenol Improves Fatty Acid Metabolism Through NHR-49/FAT-7 Suppression and Potent AAK-2 Activation inInternational journal of molecular sciences · 2026Article
- RNA methyltransferase CMTR-1 inhibition activates a GATA transcription factor-mediated protective immune response.bioRxiv : the preprint server for biology · 2025Article
- Bacterial metabolism of tryptophan causes toxicity inbioRxiv : the preprint server for biology · 2025Article
- An acyltransferase protectsbioRxiv : the preprint server for biology · 2025Article
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Abstract
Gut microbes play a crucial role in modulating host lifespan. However, the microbial factors that influence host longevity and their mechanisms of action remain poorly understood. Using the expression of Caenorhabditis elegans FAT-7, a stearoyl-CoA 9-desaturase, as a proxy for lifespan modulation, we conduct a genome-wide bacterial mutant screen and identify 26 Escherichia coli mutants that enhance host lifespan. Transcriptomic and biochemical analyses reveal that these mutant diets induce oxidative stress and activate the mitochondrial unfolded protein response (UPRmt). Antioxidant supplementation abolishes lifespan extension, confirming that oxidative stress drives these effects. The extension of lifespan requires the oxidative stress response regulators SKN-1, SEK-1, and HLH-30. Mechanistically, these effects are linked to reduced iron availability, as iron supplementation restores FAT-7 expression, suppresses UPRmt activation, and abolishes lifespan extension. Iron chelation mimics the pro-longevity effects of the mutant diets, highlighting dietary iron as a key modulator of aging. Our findings reveal a bacterial-host metabolic axis that links oxidative stress, iron homeostasis, and longevity in C. elegans.
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