Evidence map›Paper›PMID 41781676›Full record

ArticleNature aging2026

ACSS2 maintains oligodendrocyte progenitor cell pool and is required for myelination during development and aging.

Weijie Gao, Siyi Chen, Yufei Huang, Xin Wu, Lvping Zhuang, Yuying Zheng, Xiaoman Dai, Ying Fu, Wanjin Chen, Qinyong Ye and 2 more

Abstract read
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In one paragraph

Article in Nature aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

12 authors.

Weijie Gao *Department of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, Fuzhou, China.
Siyi Chen *Department of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, Fuzhou, China.
Yufei HuangDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, Fuzhou, China.
Xin WuDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, Fuzhou, China.
Lvping ZhuangDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, Fuzhou, China.
Yuying ZhengDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, Fuzhou, China.
Xiaoman DaiDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, Fuzhou, China.
Ying FuDepartment of Neurology and Institute of Neurology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Wanjin ChenDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, Fuzhou, China.
Qinyong YeDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, Fuzhou, China.
Xiaochun ChenDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, Fuzhou, China. chenxc998@fjmu.edu.cn.ORCID http://orcid.org/0000-0002-2665-4155
Jing ZhangDepartment of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, Fuzhou, China. drzj@fjmu.edu.cn.ORCID http://orcid.org/0000-0003-4037-9855

Funding

National Natural Science Foundation of China (National Science Foundation of China) Grant No. 8243004 (to XCC)National Natural Science Foundation of China (National Science Foundation of China) No. 82430041 (to XCC)
6 · The paper itself

Abstract

The reduction in number and decreased differentiation capacity of oligodendrocyte progenitor cells (OPCs) directly affect myelination in demyelinating diseases and aging, but the underlying mechanisms remain incompletely characterized. Here we observed a marked decline in the number of OPCs during aging, notably within the subpopulation highly expressing Acss2, which encodes acetyl-CoA synthetase 2 (ACSS2). Deletion of ACSS2 in the oligodendrocyte lineage resulted in a reduced OPC population, defective myelinogenesis during development, impaired myelin maintenance in adulthood and aging, and exacerbated age-related cognitive deficits. Mechanistically, ACSS2-mediated acetylation of H4K12 and H3K27 enhances the expression of Gria2, an AMPA receptor subunit critical for OPC proliferation. Furthermore, supplementation with the ACSS2 substrate acetate preserved the number of OPCs, promoted remyelination after injury and improved cognitive function in aged mice. Together, our findings highlight the essential role of ACSS2-mediated acetate utilization in maintaining the OPC population and promoting myelin production during development, demyelination and aging.

Indexed as

Acetate-CoA LigaseAgingMyelin SheathOligodendrocyte Precursor CellsOligodendrogliaAnimalsCell DifferentiationCell ProliferationDemyelinating DiseasesMiceReceptors, AMPARemyelinationAcetate-CoA LigaseReceptors, AMPA

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.