ArticleAging cell2019
Diet restriction-induced healthy aging is mediated through the immune signaling component ZIP-2 in Caenorhabditis elegans.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- An atlas of thebioRxiv : the preprint server for biology · 2026Article
- Application ofBiomolecules & therapeutics · 2026Review
- Multilayered regulation of longevity in Caenorhabditis elegans.Molecules and cells · 2026Review
- Review
- Eukaryotic Elongation Factor 2 Kinase EFK-1/eEF2K promotes starvation resistance by preventing oxidative damage in C. elegans.Nature communications · 2025Article
- Gut microbiome speciesCurrent research in microbial sciences · 2025Article
- Mitochondrial p38 Mitogen-Activated Protein Kinase: Insights into Its Regulation of and Role in LONP1-Deficient Nematodes.International journal of molecular sciences · 2023Article
- Longevity through diet restriction and immunity.BMB reports · 2023Review
- The innate immune signaling component FBXC-58 mediates dietary restriction effects on healthy aging inAging · 2023Article
- Endocytic coelomocytes are required for lifespan extension by axenic dietary restriction.PloS one · 2023Article
- Histone deacetylase HDA-1 modulates mitochondrial stress response and longevity.Nature communications · 2020Article
- Article
- Diet restriction-induced healthy aging is mediated through the immune signaling component ZIP-2 in Caenorhabditis elegans.Aging cell · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dietary restriction (DR) robustly delays the aging process in all animals tested so far. DR slows aging by negatively regulating the target of rapamycin (TOR) and S6 kinase (S6K) signaling pathway and thus inhibiting translation. Translation inhibition in C. elegans is known to activate the innate immune signal ZIP-2. Here, we show that ZIP-2 is activated in response to DR and in feeding-defective eat-2 mutants. Importantly, ZIP-2 contributes to the improvements in longevity and healthy aging, including mitochondrial integrity and physical ability, mediated by DR in C. elegans. We further show that ZIP-2 is activated upon inhibition of TOR/S6K signaling. However, DR-mediated activation of ZIP-2 does not require the TOR/S6K effector PHA-4/FOXA. Furthermore, zip-2 was not activated or required for longevity in daf-2 mutants, which mimic a low nutrition status. Thus, DR appears to activate ZIP-2 independently of PHA-4/FOXA and DAF-2. The link between DR, aging, and immune activation provides practical insight into the DR-induced benefits on health span and longevity.
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