Fasting in C. elegans required PRDX-2 and PRDX-6 for redox-linked mitochondrial and lipid remodelling
In the nematode Caenorhabditis elegans, a repeated 4-hour fasting protocol extended lifespan and reduced age-related lipofuscin and lipid accumulation; these responses were abolished in prdx-2 and prdx-6 mutants, which showed persistent redox imbalance and disrupted DAF-16 and SKN-1 signalling. [1]
Automatic summary · not editorially reviewed
The key findings
A 4-hour fasting protocol over 5 days in Caenorhabditis elegans extended lifespan, improved late-life physiological activity and reduced age-related lipofuscin and lipid accumulation. [1]
In prdx-2 and prdx-6 mutant strains, the adaptive responses were abolished, with persistent redox imbalance, mitochondrial fragmentation, altered stress resistance and disrupted DAF-16 and SKN-1 signalling. [1]
The findings identify PRDX-2 and PRDX-6 as redox sensors that translate a fasting-induced transient ROS signature into mitochondrial and lipid remodelling pathways to promote healthy ageing. [1]
The source at a glance
- Study type / format
- Preclinical experimental study in Caenorhabditis elegans (abstract)
- Population / context
- Caenorhabditis elegans nematodes, including prdx-2 and prdx-6 mutant strains
- Summary based on
- Study abstract
- Original publication
- May 22, 2026
Repeated 4-hour fasting in C. elegans
The abstract describes a 4-hour fasting protocol applied over 5 days in the nematode Caenorhabditis elegans. This protocol extended lifespan, improved late-life physiological activity and reduced age-related lipofuscin and lipid accumulation. The fasting protocol produced a transient increase in mitochondrial reactive oxygen species (ROS), promoted mitochondrial turnover and attenuated age-related mitochondrial fragmentation. These adaptive responses required activation and nuclear localisation of the stress-responsive transcription factors DAF-16/FOXO and SKN-1/Nrf2.
Supporting source [1]
prdx-2 and prdx-6 mutants lost fasting responses
In prdx-2 and prdx-6 mutant strains, these adaptive responses were abolished. The mutants exhibited persistent redox imbalance, mitochondrial fragmentation, altered stress resistance and disrupted DAF-16 and SKN-1 signalling. Mechanistically, loss of 2-Cys PRDX-2 impaired activation of the p38 MAPK PMK-1 pathway, resulting in defective SKN-1 activation. In contrast, loss of 1-Cys PRDX-6 disrupted lipid metabolic signalling, preventing induction of NHR-80 and downstream fatty acid desaturases required for metabolic adaptations. Despite distinct initial signalling pathways, both peroxiredoxins converged on regulation of DAF-16 and SKN-1.
Supporting source [1]
Abstract-only scope of the C. elegans findings
The abstract identifies PRDX-2 and PRDX-6 as redox sensors that translate a fasting-induced transient ROS signature into mitochondrial and lipid remodelling pathways to promote healthy ageing. These findings come from the nematode Caenorhabditis elegans, not from humans. The abstract does not report sample sizes, replication or the full experimental detail, and the full text was not reviewed. The described lifespan and physiological effects are associations with the fasting protocol in this model, not established causal benefits for human health.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings are from the nematode Caenorhabditis elegans, not humans. Sample sizes, replication and full experimental detail are not reported in the abstract.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Li P, Zheng Y, Casas-Martinez JC, Xia Q, Miranda-Vizuete A, Goljanek-Whysall K, McDonagh B. · europepmc.org · May 22, 2026