Evidence map›Paper›PMID 40133712›Full record

ArticleScience China. Life sciences2025

RIG-I-driven CDKN1A stabilization reinforces cellular senescence.

Cui Wang, Xiaoyu Jiang, Hong-Yu Li, Jianli Hu, Qianzhao Ji, Qiaoran Wang, Xiaoqian Liu, Daoyuan Huang, Kaowen Yan, Liyun Zhao and 7 more

Abstract read
PubMed Publisher
In one paragraph

Article in Science China. Life sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
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  7. Article
  8. Review
  9. Biomarkers of ageing of humans and non-human primates.Nature reviews. Molecular cell biology · 2025
    Review
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  11. Review
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

17 authors.

Cui Wang *China National Center for Bioinformation, Beijing, 100101, China.
Xiaoyu Jiang *State Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
Hong-Yu Li *Key Laboratory of Biomacromolecules (CAS), National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
Jianli HuChina National Center for Bioinformation, Beijing, 100101, China.
Qianzhao JiState Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
Qiaoran WangChina National Center for Bioinformation, Beijing, 100101, China.
Xiaoqian LiuState Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
Daoyuan HuangAdvanced Innovation Center for Human Brain Protection, National Clinical Research Center for Geriatric Disorders, Xuanwu Hospital Capital Medical University, Beijing, 100053, China.
Kaowen YanState Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
Liyun ZhaoAdvanced Innovation Center for Human Brain Protection, National Clinical Research Center for Geriatric Disorders, Xuanwu Hospital Capital Medical University, Beijing, 100053, China.
Yanling FanChina National Center for Bioinformation, Beijing, 100101, China.
Si WangAdvanced Innovation Center for Human Brain Protection, National Clinical Research Center for Geriatric Disorders, Xuanwu Hospital Capital Medical University, Beijing, 100053, China.
Shuai MaState Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
Juan Carlos Izpisua BelmonteAltos Labs, Inc., San Diego, CA, 94022, USA.
Jing QuState Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China. qujing@ioz.ac.cn.
Guang-Hui LiuState Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China. ghliu@ioz.ac.cn.
Weiqi ZhangChina National Center for Bioinformation, Beijing, 100101, China. zhangwq@big.ac.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The innate immune signaling network follows a canonical format for signal transmission. The innate immune pathway is crucial for defense against pathogens, yet its mechanistic crosstalk with aging processes remains largely unexplored. Retinoic acid-inducible gene-I (RIG-I), a key mediator of antiviral immunity within this pathway, has an enigmatic role in stem cell senescence. Our study reveals that RIG-I levels increase in human genetic and physiological cellular aging models, and its accumulation drives cellular senescence. Conversely, CRISPR/Cas9-mediated RIG-I deletion or pharmacological inhibition in human mesenchymal stem cells (hMSCs) confers resistance to senescence. Mechanistically, RIG-I binds to endogenous mRNAs, with CDKN1A mRNA being a prominent target. Specifically, RIG-I stabilizes CDKN1A mRNA, resulting in elevated CDKN1A transcript levels and increased p21

Indexed as

Cellular SenescenceCyclin-Dependent Kinase Inhibitor p21DEAD Box Protein 58CRISPR-Cas SystemsHumansImmunity, InnateMesenchymal Stem CellsReceptors, ImmunologicRNA, MessengerSignal TransductionCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DEAD Box Protein 58Receptors, ImmunologicRIGI protein, humanRNA, Messengeraginghuman stem cellinnate immune pathwayRIG-Isenescence

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.