Evidence map›Paper›PMID 39935344›Full record

ArticleAging cell2025

Reduction of DNA Topoisomerase Top2 Reprograms the Epigenetic Landscape and Extends Health and Life Span Across Species.

Man Zhu, Meng Ma, Lunan Luo, Feiyang Li, Jiashun Zheng, Yan Pan, Lu Yang, Ying Xiao, Ziyan Wang, Bo Xian and 3 more

Abstract read
In one paragraph

Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. The Roles of Topoisomerases in Transcriptional Regulation.International journal of molecular sciences · 2026
    Review
  4. 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.

Man ZhuDepartment of Health Management & Institute of Health Management, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.ORCID 0009-0007-4610-105X
Meng MaLaboratory of Aging Research, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Lunan LuoLaboratory of Aging Research, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Feiyang LiLaboratory of Aging Research, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Jiashun ZhengDepartment of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California, USA.
Yan PanLaboratory of Aging Research, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Lu YangLaboratory of Aging Research, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Ying XiaoLaboratory of Aging Research, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Ziyan WangLaboratory of Aging Research, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Bo XianLaboratory of Aging Research, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Yi ZhengDepartment of Health Management & Institute of Health Management, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Hao LiDepartment of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California, USA.
Jing YangDepartment of Health Management & Institute of Health Management, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.

Funding

Sichuan Province Science and Technology Support Program 2023YFS0050Sichuan Province Science and Technology Support Program 2024YFHZ0009Sichuan Province Science and Technology Support Program 23NSFSC0349University of Electronic Science and Technology of China and China West Hospital ZYGX2022YGRH018
6 · The paper itself

Abstract

DNA topoisomerases are essential molecular machines that manage DNA topology in the cell and play important roles in DNA replication and transcription. We found that knocking down the enzyme topoisomerase Top2 or its mammalian homolog TOP2B increases the lifespan of S. cerevisiae, C. elegans, and mice. TOP2B reduction also extends the health span of mice and alleviates the pathologies of aging in multiple tissues. At the cellular/molecular level, TOP2B reduction alleviates the major hallmarks of aging, including senescence, DNA damage, and deregulated nutrient sensing. We observed that TOP2B reduction changes the epigenetic landscape of various tissues in old mice toward that of the young animals, and differentially downregulates genes with active promoter and high expression. Our observations suggest that Top2 reduction confers pro-longevity effect across species possibly through a conserved mechanism and may be a promising strategy for longevity intervention.

Indexed as

DNA Topoisomerases, Type IIEpigenesis, GeneticLongevityAgingAnimalsCaenorhabditis elegansHumansMiceSaccharomyces cerevisiaeDNA Topoisomerases, Type IIagingessential genehistone modificationlongevitytopoisomerase II

Identifiers

PMID39935344
PMCPMC12151872

What OpenQuestion holds

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LicenceCC BY
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 OpenQuestion graph.