Peroxisomal enzyme ACOX-1.2 enables extended lifespan in long-lived roundworms
Inhibiting the fatty acid oxidation enzyme suppresses both autophagy and longevity in long-lived rsks-1 mutant Caenorhabditis elegans.
Current issues in molecular biology · Zhao Q et al. · Paper published 4 Sep 2026
In Caenorhabditis elegans, researchers assessed reactive oxygen species levels across five long-lived mutant strains using four distinct probes. They observed elevated hydrogen peroxide levels specifically in rsks-1 mutants. Transcriptomic analysis revealed that genes involved in peroxisomal fatty acid beta-oxidation were upregulated in this strain. The team determined that the peroxisomal enzyme ACOX-1.2 regulates this shift in hydrogen peroxide metabolism. Furthermore, lifespan assays and genetic tests showed that knocking down acox-1.2 via RNA interference suppressed the increased autophagy and lifespan seen in rsks-1 worms. These results establish that peroxisomal fatty acid beta-oxidation helps govern longevity regulation in this invertebrate model.
Why it matters
The findings identify peroxisomal fatty acid beta-oxidation as a key metabolic driver of autophagy and longevity regulation in aging biology.
Caveats
This research was conducted exclusively in Caenorhabditis elegans, and the effects were identified in a specific mutant genetic background.
Written from the paper’s abstract, and every claim checked against it before publishing. Read the paper for the full methods and data.
The paper
The Extended Lifespan of Caenorhabditis elegans rsks-1 Mutants Depends on the Peroxisomal Fatty Acid β-Oxidation Enzyme ACOX-1.2
Zhao Q, Zhu R, Guo HX et al.
Current issues in molecular biology · 4 Sep 2026 · Peer-reviewed
- Relevance
- Core geroscience
- News value
- Notable
- Evidence
- Model organisms
- Status
- Peer-reviewed
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