Evidence map›Paper›PMID 39827045›Full record

ArticleChinese journal of traumatology = Zhonghua chuang shang za zhi2026

Multiomics analysis elucidated the role of inflammatory response and bile acid metabolism disturbance in electric shock-induced liver injury in mice.

Wenjuan Zhang, Luncai Yin, Hui Wang, Ce Long, Jin Liu, Ping Deng, Yang Yue, Jingdian Li, Mindi He, Yonghui Lu and 10 more

Abstract read
In one paragraph

Article in Chinese journal of traumatology = Zhonghua chuang shang za zhi, 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. Article
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

20 authors.

Wenjuan ZhangDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Luncai YinDepartment of Oncology, Affiliated Dazu Hospital of Chongqing Medical University, Chongqing, 402360, China.
Hui WangNuclear Medicine Department, General Hospital of Tibet Military Area Command, Lhasa, 850007, Xizang, China.
Ce LongGeneral Hospital of Xizang Military Area Command, Lhasa, 850007, Xizang, China.
Jin LiuCardiovascular Department, General Hospital of Xizang Military Area Command, Lhasa, 850007, Xizang, China.
Ping DengDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Yang YueDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Jingdian LiDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Mindi HeDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Yonghui LuDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Yan LuoDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Siyu ChenDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Jiawen TaoDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Li TianDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Jia XieDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Mengyan ChenDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Zhengping YuDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Zhou ZhouCenter for Neurointelligence, School of Medicine, Chongqing University, Chongqing, 400030, China.
Peng GaoDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China.
Huifeng PiDepartment of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University, Chongqing, 400038, China; State Key Laboratory of Trauma and Chemical Poisoning, Army Medical University, Chongqing, 400038, China. Electronic address: pihuifeng@tmmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeOrgan damage caused by electric shock has attracted great attention. Some animal investigations and clinical cases have suggested that electric shock can induce liver injury. This study aimed to investigate the potential mechanism of liver injury induced by electric shock.

methodsHealthy male C57BL/6J mice aged 6-8 weeks were romandly divided into 2 groups: control group and electric shock group. Mice in the electric shock group were shocked on the top of the skull with an electric baton (20 kV) for 5 sec, while mice in the control group were exposed to only the acoustic and light stimulation produced by the electric baton. The effect of electric shock on liver function was evaluated by histological and biochemical analysis, and a metabolomics and transcriptomics study was performed to investigate how electric shock might induce liver damage. All data of this study were analyzed using a 2-tailed unpaired Student's t-test in SPSS 22.0 Statistical Package.

resultsThe electric shock group had significantly higher serum aspartate aminotransferase and alanine aminotransferase levels than the control group (p < 0.001), and the shock notably caused cytoplasmic swelling and vacuolization, mild inflammatory cell (mainly macrophages and monocytes) infiltration and acute focal necrosis in hepatocytes (p < 0.001). A total of 47 differential metabolites and 249 differentially expressed genes (DEGs) were detected using metabolomic and transcriptomic analyses. These differential metabolites were significantly enriched in primary bile acid biosynthesis (p < 0.05). Gene ontology functional analysis of the DEGs revealed that electric shock disturbed a key biological process involved in the inflammatory response in the mouse liver, and a significant number of DEGs were enriched in Kyoto Encyclopedia of Genes and Genomes-identified pathways related to inflammation, such as the interleukin-17, tumor necrosis factor and mitogen-activated protein kinase signalling pathway. Transcriptomic and metabolomic analyses revealed that bile acid metabolism disturbance including up-regulation of the taurochenodesoxycholic acid, chenodeoxycholic acid and taurocholic acid, and down-regulation of chenodeoxycholic acid clycine conjugate may contribute to the electric shock-induced inflammatory response.

conclusionElectric shock can induce liver inflammatory injury through the interleukin-17, tumor necrosis factor, and mitogen-activated protein kinase signaling pathway, and the bile acid metabolism disturbance including up-regulation of the taurochenodesoxycholic acid, chenodeoxycholic acid and taurocholic acid, and down-regulation of chenodeoxycholic acid clycine conjugate may contribute to inflammatory liver injury following electric shock.

Indexed as

Bile Acids and SaltsElectric InjuriesInflammationLiverAlanine TransaminaseAnimalsAspartate AminotransferasesMaleMetabolomicsMiceMice, Inbred C57BLMultiomicsAlanine TransaminaseAspartate AminotransferasesBile Acids and SaltsBile acid metabolismElectric shockInflammationLiver injuryMetabolomicsTranscriptomics

Identifiers

PMID39827045
PMCPMC12891842

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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.