Evidence map›Paper›PMID 42497212›Full record

ArticlePLoS computational biology2026

Cell-type-specific m1A dynamics are associated with microglial phenotypic transition and neuronal metabolic adaptation during spinal cord injury.

Chi Zhang, Shaolong Li, Ruizhi Jiang, Heng Duan, Chuang Li, Enlin Qi, Mingxin Wu, Xueying Li, Shiqing Feng, Hengxing Zhou

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PLoS computational biology, 2026. 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

10 authors.

Chi ZhangDepartment of Orthopaedics, The Second Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Cheeloo College of Medicine, Shandong University, Jinan, China.
Shaolong LiDepartment of Orthopaedics, Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, China.
Ruizhi JiangDepartment of Orthopaedics, Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, China.
Heng DuanDepartment of Orthopaedics, Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, China.
Chuang LiDepartment of Orthopaedics, The Second Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Cheeloo College of Medicine, Shandong University, Jinan, China.
Enlin QiDepartment of Orthopaedics, Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, China.
Mingxin WuDepartment of Orthopaedics, Tianjin Medical University General Hospital, International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin Key Laboratory of Spine and Spinal Cord, Tianjin, China.
Xueying LiShandong University Centre for Orthopaedics, Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, China.
Shiqing FengDepartment of Orthopaedics, The Second Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Cheeloo College of Medicine, Shandong University, Jinan, China.
Hengxing ZhouDepartment of Orthopaedics, Qilu Hospital of Shandong University, Shandong University Centre for Orthopaedics, Advanced Medical Research Institute, Cheeloo College of Medicine, Shandong University, Jinan, China.ORCID https://orcid.org/0000-0003-0053-8970

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

m1A (N1-methyladenosine) is an important epigenetic mechanism that regulates the onset and progression of many diseases, including spinal cord injury (SCI). To investigate the overall changes in m1A following SCI, we analyzed transcriptomic sequencing data from SCI samples and assigned m1A scores based on the levels of m1A regulatory factors. In this study, the m1A score is an inferred proxy calculated from the expression of m1A regulator genes (writers/erasers/readers). It does not directly measure RNA m1A modification levels. Our results show that the m1A score increased within the first day after SCI and then decreased, falling below baseline by day 3 and day 7. Further analysis revealed that microglia and neurons are the two cell types with the most significant changes in the m1A score. In microglia, m1A score decreased at all time points, whereas in neurons, m1A score increased at all time points. Additionally, pseudotime and functional enrichment analyses suggested that the m1A score is associated with microglial phenotypic transition and neuronal energy metabolism, which was further validated by both in vivo and in vitro experiments. In summary, our study unveils the characteristic changes of m1A at both the bulk and single-cell levels following SCI, and suggests potential links to neuronal function and supports the rationale for further studies exploring m1A-related regulators as therapeutic targets in SCI.

Indexed as

AdenosineMicrogliaNeuronsSpinal Cord InjuriesAdaptation, PhysiologicalAnimalsComputational BiologyEpigenesis, GeneticEpitranscriptomeGene Expression ProfilingMicePhenotypeRNA MethylationTranscriptomeAdenosineN-methyladenosine

Identifiers

PMID42497212
PMCPMC13423174

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LicenceCC BY
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Registered trials

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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.