Evidence map›Paper›PMID 42070156›Full record

ArticleAging cell2026

Vitamin K2 Extends Lifespan by Alleviating Mitochondrial Stress via the JNK-1/SIR-2.1/DAF-16 Signaling Axis in Caenorhabditis elegans.

Song-Yu Guo, Yu-Qi Li, Hua Piao, Wen-Fei Zheng, Si-Qi Li, Ze-Yang Liu, Jun-Ting Lv, Yue Kong, Qi-Fa Li, Ying-Zi Wang and 3 more

Abstract read
In one paragraph

Article in Aging cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

13 authors.

Song-Yu GuoDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Yu-Qi LiDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Hua PiaoDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Wen-Fei ZhengDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Si-Qi LiDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Ze-Yang LiuDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Jun-Ting LvDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Yue KongDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Qi-Fa LiDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Ying-Zi WangDepartment of International Medical Services, Second Affiliated Hospital of Dalian Medical University, Dalian, China.ORCID https://orcid.org/0000-0002-6540-2428
Shu-Zhuang LiDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.
Chun-Li ZhaoDepartment of Critical Care Medicine, Affiliated Dalian Friendship Hospital of Dalian Medical University, Dalian, China.
Shao LiDepartment of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, Liaoning, China.ORCID https://orcid.org/0000-0002-4889-8636

Funding

DMU&DLBL 2026JCYJ-02The Leading Talent Team Project of the Education Department of Liaoning Province LJ222510161002The National Natural Sciences Foundation of China 82101661The National Natural Sciences Foundation of China 82401823The National Natural Sciences Foundation of China 82471464
6 · The paper itself

Abstract

Vitamin K2 is a fat-soluble vitamin that has been reported to exhibit significant anti-stress activity. Anti-stress properties are considered to be closely associated with lifespan extension. Therefore, we investigated the effects of vitamin K2 on the lifespan and stress resistance of Caenorhabditis elegans, as well as the underlying mechanisms. In the present study, we found that the effects of Vitamin K2 on C. elegans are concentration-dependent. High concentrations (10 μM) of Vitamin K2 are toxic to C. elegans, whereas lower concentrations (5 μM) are beneficial. Treatment with 5 μM Vitamin K2 can extend the lifespan of C. elegans, enhance its physiological functions, protect the intestinal barrier, and reduce the accumulation of lipofuscin associated with aging. Furthermore, Vitamin K2 enhanced the stress resistance of C. elegans by maintaining mitochondrial morphology, alleviating mitochondrial stress, reducing ROS levels, and improving mitochondrial membrane potential and ATP production. Vitamin K2 activates the JNK-1/SIR-2.1/DAF-16 signaling pathway and upregulates the expression of downstream target genes such as ctl-1, ctl-2, sod-1, sod-3, and hsp-16.2. We conclude that appropriate doses of Vitamin K2 protect C. elegans from senescence by activating the JNK-1/SIR-2.1/DAF-16-mediated anti-mitochondrial oxidative stress pathway. These findings suggest that Vitamin K2 may have beneficial effects on lifespan and mitochondrial health in C. elegans, providing a basis for further investigation into its potential relevance for aging and age-related diseases in more complex model systems.

Indexed as

Caenorhabditis elegansCaenorhabditis elegans ProteinsLongevityMitochondriaMitogen-Activated Protein Kinase 8SirtuinsTranscription FactorsVitamin K 2AnimalsForkhead Transcription FactorsMembrane Potential, MitochondrialMitogen-Activated Protein KinasesOxidative StressReactive Oxygen SpeciesSignal TransductionStress, PhysiologicalCaenorhabditis elegans Proteinsdaf-16 protein, C elegansForkhead Transcription FactorsJNK-1 protein, C elegansMitogen-Activated Protein Kinase 8Mitogen-Activated Protein KinasesReactive Oxygen SpeciesSIR-2.1 protein, C elegansSirtuinsTranscription FactorsVitamin K 2Caenorhabditis elegansextended the lifespanJNK/SIR‐2.1/DAF‐16 pathwaymitochondrial stressvitamin K2

Identifiers

PMID42070156
PMCPMC13135748

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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.