Evidence map›Paper›PMID 39779477›Full record

ArticleJournal of cellular and molecular medicine2025

Untargeted Metabolomics Reveals Metabolic Link Between Histone H3K27 Demethylase UTX and Neurodevelopment.

Lin Chen, Maozhu Liu, Xinhua Dai, Cuilin He, Kejing Wang, Jinhua Tang, Yang Yang

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2025. 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. Discovery and structural studies of histone demethylases.Frontiers in epigenetics and epigenomics · 2025
    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

7 authors.

Lin ChenDepartment of Pharmacy, Chongqing Health Center for Women and Children, Women and Children's Hospital of Chongqing Medical University, Chongqing, China.
Maozhu LiuCenter of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, China.
Xinhua DaiDepartment of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, China.
Cuilin HeDepartment of Pharmacy, The First People's Hospital of Shuangliu District, Chengdu, China.
Kejing WangDepartment of Pharmacy, Chongqing Health Center for Women and Children, Women and Children's Hospital of Chongqing Medical University, Chongqing, China.
Jinhua TangDepartment of Pharmacy, Chongqing Health Center for Women and Children, Women and Children's Hospital of Chongqing Medical University, Chongqing, China.
Yang YangDepartment of Pharmacy, Chongqing Health Center for Women and Children, Women and Children's Hospital of Chongqing Medical University, Chongqing, China.ORCID 0009-0000-0268-0124

Funding

Chongqing science technology commission of China CSTB2023NSCQ-MSX0267Development Support Program for Future Medical Youth Innovation Teams of Chongqing Medical University WO208
6 · The paper itself

Abstract

Ubiquitously transcribed tetratricopeptide repeat on chromosome X (UTX) is a chromatin modifier responsible for regulating the demethylation of histone H3 lysine 27 trimethylation (H3K27me3), which is crucial for human neurodevelopment. To date, the impact of UTX on neurodevelopment remains elusive. Therefore, this study aimed to investigate the potential molecular mechanisms underlying the effects of UTX on neurodevelopment through untargeted metabolomics based on ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). We found that UTX knockout in neurones leads to cell death and apoptosis in the hippocampus and cortex, as well as induces impaired learning and memory functions in mice. Moreover, UTX deletion contributed to significant metabolic perturbations in brain tissues. A total of 223 differential metabolites were identified between wild-type (WT) and UTX cKO mice. Pathway analysis indicated that the metabolic pathways mainly affected by UTX deletion were alanine, aspartate, and glutamate metabolism, resulting in significant alterations in L-alanine, L-aspartate, D-aspartate, N-acetylaspartylglutamate, L-glutamate, and argininosuccinic acid. These data emphasised that UTX may exert a key effect in neurodevelopment and that the underlying mechanism may be related to the regulation of the alanine, aspartate, and glutamate metabolism pathways, especially the characteristic metabolites involved in this pathway.

Indexed as

Histone DemethylasesMetabolomicsMice, KnockoutAnimalsApoptosisBrainHippocampusHistonesMaleMetabolic Networks and PathwaysMetabolomeMiceMice, Inbred C57BLNeuronsTandem Mass SpectrometryHistone DemethylasesHistonesUtx protein, mousemetabolic pathwaymetabolomicsneurodevelopmentUTX

Identifiers

PMID39779477
PMCPMC11710934

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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.