Evidence map›Paper›PMID 42898715›Full record

ArticleGenes & diseases2027

Glis1 regulates metabolic programming by promoting H3K18 lactylation to alleviate neuronal senescence following spinal cord injury.

Dachuan Li, Xiao Lu, Zhaoyang Gong, Jianwei Wu, Yuxuan Zhang, Jiongdong Wu, Chenpei Xu, Xingyu Guo, Guangyu Xu, Haocheng Xu and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes & diseases, 2027. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

22 authors.

Dachuan LiDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Xiao LuDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Zhaoyang GongDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Jianwei WuDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Yuxuan ZhangDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Jiongdong WuDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Chenpei XuDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Xingyu GuoDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Guangyu XuDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Haocheng XuDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Shuo YangDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Xinlei XiaDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Feizhou LuDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Jianyuan JiangDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Shihao LuDepartment of Orthopedics, Changhai Hospital, Navy Medical University, Shanghai 200433, China.
Junzhe ShengDepartment of Spinal Surgery, Changzheng Hospital, Navy Medical University, Shanghai 200003, China.
Xiaosheng MaDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Wei ZhuDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Fei ZouDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Chi SunDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.
Xiaochuan GuDepartment of Orthopedics, Changhai Hospital, Navy Medical University, Shanghai 200433, China.
Yunzhi GuanDepartment of Orthopedics, Huashan Hospital, Fudan University, Shanghai 200040, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal senescence is a significant factor impeding spinal cord injury (SCI) repair. Research indicates that Glis1, a Kruppel-like zinc finger transcription factor, is pivotal in reprogramming senescent cells and enhancing genomic stability via lactylation. Histone lactylation, an epigenetic modification using lactate as a substrate, becomes prominent post-SCI due to increased neuronal lactate levels. However, the mechanisms linking neuronal senescence and histone lactylation following SCI remain poorly understood. This study elucidates the roles of Glis1, H3K18 lactylation, and neuronal senescence through comprehensive

Indexed as

Cellular senescenceHistone proteinsLactylationMetabolic reprogrammingSCI

Identifiers

PMID42898715
PMCPMC13678048

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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.