Evidence map›Paper›PMID 40388671›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Histone Lactylation Antagonizes Senescence and Skeletal Muscle Aging by Modulating Aging-Related Pathways.

Fanju Meng, Jianuo He, Xuebin Zhang, Wencong Lyu, Ran Wei, Shiyi Wang, Zhehao Du, Haochen Wang, Jinlong Bi, Xueyang Hua and 7 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Lactate-Mediated Lysine Lactylation in Renal Fibrosis: Current Progress and Challenges.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  5. Article
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  9. Article
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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.

Fanju MengThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.ORCID https://orcid.org/0009-0001-7918-6666
Jianuo HeThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.ORCID https://orcid.org/0009-0006-8826-8408
Xuebin ZhangThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.ORCID https://orcid.org/0000-0002-0563-6994
Wencong LyuThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.
Ran WeiThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.
Shiyi WangThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.
Zhehao DuThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.
Haochen WangThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.
Jinlong BiThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.
Xueyang HuaHefei National Laboratory for Physical Sciences at the Microscale, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230026, China.
Chao ZhangKunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, China.
Yiting GuanZhanjiang Institute of Clinical Medicine, Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang, 524045, China.
Guoliang LyuThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.
Xiao-Li TianDepartment of Human Population Genetics, Human Aging Research Institute (HARI) and School of Life Sciences, Nanchang University, Nanchang, 330031, China.
Lijun ZhangThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.
Wenbing XieHefei National Laboratory for Physical Sciences at the Microscale, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230026, China.ORCID https://orcid.org/0000-0003-2546-2415
Wei TaoThe State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing, 100871, China.ORCID https://orcid.org/0000-0002-1860-895X

Funding

National Key Research and Development Program of China 2021YFA0909300National Key Research and Development Program of China 2023YFC3603300National Natural Science Foundation of China 32241006National Natural Science Foundation of China 82192891
6 · The paper itself

Abstract

Epigenetic alterations are among the prominent drivers of cellular senescence and/or aging, intricately orchestrating gene expression programs during these processes. This study shows that histone lactylation, plays a pivotal role in counteracting senescence and mitigating dysfunctions of skeletal muscle in aged mice. Mechanistically, histone lactylation and lactyl-CoA levels markedly decrease during cellular senescence but are restored under hypoxic conditions primarily due to elevated glycolytic activity. The enrichment of histone lactylation at promoters is essential for sustaining the expression of genes involved in the cell cycle and DNA repair pathways. Furthermore, the modulation of enzymes crucial for histone lactylation, leads to reduced histone lactylation and accelerated cellular senescence. Consistently, the suppression of glycolysis and the depletion of histone lactylation are also observed during skeletal muscle aging. Modulating the enzymes can also lead to the loss of histone lactylation in skeletal muscle, downregulating DNA repair and proteostasis pathways and accelerating muscle aging. Running exercise increases histone lactylation, which in turn upregulate key genes in the DNA repair and proteostasis pathways. This study highlights the significant roles of histone lactylation in modulating cellular senescence as well as muscle aging, providing a promising avenue for antiaging intervention via metabolic manipulation.

Indexed as

AgingCellular SenescenceHistonesMuscle, SkeletalAnimalsDNA RepairEpigenesis, GeneticMaleMiceMice, Inbred C57BLHistonesepigeneticshistone lactylationsenescenceskeletal muscle aging

Identifiers

PMID40388671
PMCPMC12165025

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.