Evidence map›Paper›PMID 42030644›Full record

ArticleRedox biology2026

Early-life redox perturbation programs intergenerational redox vulnerability through DAF-16/FOXO and SKN-1/Nrf2 signaling in Caenorhabditis elegans.

Jingyimei Liang, Yuxuan Zhao, Yitong Xie, Yazhuo Li, Wanning Ma, Boya Ouyang, Hui Cao, Yahong Yuan, Tianli Yue, Jianbo Xiao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Jingyimei LiangCollege of Food Science and Technology, Northwest University, Xi'an, 710069, China; Universidade de Vigo, Nutrition and Bromatology Group, Department of Analytical Chemistry and Food Science, Faculty of Science, Ourense, 32004, Spain; Instituto de Agroecoloxía e Alimentación (IAA), Universidade de Vigo, Campus Auga, Ourense, 32004, Spain; Key Laboratory of Food Safety of Shaanxi Provincial Higher Education Institutions, Northwest University, Xi'an, 710069, China.
Yuxuan ZhaoUniversidade de Vigo, Nutrition and Bromatology Group, Department of Analytical Chemistry and Food Science, Faculty of Science, Ourense, 32004, Spain; Instituto de Agroecoloxía e Alimentación (IAA), Universidade de Vigo, Campus Auga, Ourense, 32004, Spain.
Yitong XieCollege of Food Science and Technology, Northwest University, Xi'an, 710069, China; Key Laboratory of Food Safety of Shaanxi Provincial Higher Education Institutions, Northwest University, Xi'an, 710069, China.
Yazhuo LiCollege of Food Science and Technology, Northwest University, Xi'an, 710069, China; Key Laboratory of Food Safety of Shaanxi Provincial Higher Education Institutions, Northwest University, Xi'an, 710069, China.
Wanning MaUniversidade de Vigo, Nutrition and Bromatology Group, Department of Analytical Chemistry and Food Science, Faculty of Science, Ourense, 32004, Spain; Instituto de Agroecoloxía e Alimentación (IAA), Universidade de Vigo, Campus Auga, Ourense, 32004, Spain.
Boya OuyangUniversidade de Vigo, Nutrition and Bromatology Group, Department of Analytical Chemistry and Food Science, Faculty of Science, Ourense, 32004, Spain; Instituto de Agroecoloxía e Alimentación (IAA), Universidade de Vigo, Campus Auga, Ourense, 32004, Spain.
Hui CaoUniversidade de Vigo, Nutrition and Bromatology Group, Department of Analytical Chemistry and Food Science, Faculty of Science, Ourense, 32004, Spain; Instituto de Agroecoloxía e Alimentación (IAA), Universidade de Vigo, Campus Auga, Ourense, 32004, Spain. Electronic address: hui_cao0830@yahoo.com.
Yahong YuanCollege of Food Science and Technology, Northwest University, Xi'an, 710069, China; Key Laboratory of Food Safety of Shaanxi Provincial Higher Education Institutions, Northwest University, Xi'an, 710069, China. Electronic address: yyh@nwu.edu.cn.
Tianli YueCollege of Food Science and Technology, Northwest University, Xi'an, 710069, China; Key Laboratory of Food Safety of Shaanxi Provincial Higher Education Institutions, Northwest University, Xi'an, 710069, China. Electronic address: yuetl@nwu.edu.cn.
Jianbo XiaoUniversidade de Vigo, Nutrition and Bromatology Group, Department of Analytical Chemistry and Food Science, Faculty of Science, Ourense, 32004, Spain; Instituto de Agroecoloxía e Alimentación (IAA), Universidade de Vigo, Campus Auga, Ourense, 32004, Spain. Electronic address: jianboxiao@yahoo.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Early metabolic stress is a key factor influencing long term intergenerational adaptation in organisms. While excessive dietary methionine is known to disrupt one-carbon metabolism, it remains unclear whether early gestational methionine excess induces sustained epigenetic remodeling, thereby affecting redox stability in offspring. Using C. elegans as a model, we demonstrate that early gestational methionine excess in parental induces sustained metabolic stress in offspring, impairing their functional stability. This manifests as impaired motility, shortened lifespan, and elevated oxidative stress levels. Mechanistically, this intergenerational vulnerability is associated with metabolic reprogramming towards a serine-glycine-one-carbon axis. This leads to methyl donor imbalance and chromatin remodeling, characterized by SET-2/WDR-5.1 dependent H3K4 hypermethylation. Meanwhile, the stress response programs of DAF-16/FOXO and SKN-1/Nrf2 are restricted, thus affecting the redox adaptability of the offspring. Importantly, intervention with the dietary polyphenol epigallocatechin gallate (EGCG) can restore metabolic homeostasis and alleviate these chromatin and transcriptional restrictions. In summary, our findings reveal a metabolic and epigenetic framework by which early-life nutritional imbalances influence intergenerational redox resilience. We also emphasize that EGCG represents a potential nutritional strategy to alleviate metabolic stress caused by methionine excess.

Indexed as

Caenorhabditis elegansCaenorhabditis elegans ProteinsDNA-Binding ProteinsForkhead Transcription FactorsNF-E2-Related Factor 2Signal TransductionTranscription FactorsAnimalsCatechinEpigenesis, GeneticEpigenetic MemoryLongevityMethionineOxidation-ReductionOxidative StressCaenorhabditis elegans ProteinsCatechindaf-16 protein, C elegansDNA-Binding Proteinsepigallocatechin gallateForkhead Transcription FactorsMethionineNF-E2-Related Factor 2skn-1 protein, C elegansTranscription FactorsEarly-life metabolic stressHistone methylationLongevityOne-carbon metabolismRedox resilience

Identifiers

PMID42030644
PMCPMC13126467

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.