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.
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.
- Acox-1.2 knockdown
- RSKS-1 mutation
- Deregulated nutrient-sensing
- Disabled macroautophagy
- Autophagy
- Lipid and ceramide metabolism
- Oxidative stress and ROS signalling
- mTOR signalling
- acox-1.2
- rsks-1
- Hydrogen peroxide
- Caenorhabditis elegans
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