Evidence map›Paper›PMID 41022071›Full record

ArticleThe Journal of international medical research2025

Omics-based integrative analysis of sepsis-induced myocardial dysfunction.

Jie-Wen Zhao, Zeng-Xiang Dong, Wei Wang, Si-Qi Sheng, Kai-Jiang Yu

Abstract read
In one paragraph

Article in The Journal of international medical research, 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. 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

5 authors.

Jie-Wen ZhaoDepartments of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University, Harbin Medical University, China.
Zeng-Xiang DongKey Laboratory of Hepatosplenic Surgery, Ministry of Education, China.
Wei WangInstitute of Cardiovascular Disease, The First Affiliated Hospital of Harbin Medical University, China.
Si-Qi ShengInstitute of Cardiovascular Disease, The First Affiliated Hospital of Harbin Medical University, China.
Kai-Jiang YuDepartments of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University, Harbin Medical University, China.ORCID 0009-0009-9565-7534

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ObjectiveSepsis-induced myocardial dysfunction is a common complication of sepsis, characterized by high mortality and an unclear underlying mechanism. This study conducted an integrative multiomics analysis of mice with sepsis-induced myocardial dysfunction to provide new insights into potential mechanisms.MethodWe constructed an animal model of sepsis-induced myocardial dysfunction and analyzed the metabolomics, transcriptomics, and protein profiles of the heart tissues in the control and experimental groups.ResultsUntargeted metabolomics identified 74 significantly altered metabolites in the positive ion mode, of which 48 were upregulated and 26 downregulated; moreover, 70 significantly altered metabolites were detected in the negative ion mode, with 50 being upregulated and 20 downregulated. Transcriptomics revealed 4831 differentially expressed genes, with 3027 being downregulated and 1804 upregulated. Proteomics identified 107 significant proteins, 94 of which were significantly upregulated and 13 significantly downregulated. Integrated omics analysis revealed three significantly altered metabolites common to both groups: L-glutamate, L-aspartate, and nicotinamide. These metabolites were predominantly involved in nicotinate and nicotinamide metabolism, histidine metabolism, and nitrogen metabolism, potentially related to the pathogenesis of sepsis-induced myocardial dysfunction.ConclusionThe pathogenesis of sepsis-induced myocardial dysfunction in mice may be associated with alterations in nicotinate and nicotinamide metabolism, histidine metabolism, and nitrogen metabolism.

Indexed as

CardiomyopathiesMetabolomicsMyocardiumSepsisAnimalsDisease Models, AnimalGene Expression ProfilingMaleMiceMice, Inbred C57BLProteomicsTranscriptomemetabolic pathwaysmetabolomicsproteomicsSepsis-induced myocardial dysfunctiontranscriptomics

Identifiers

PMID41022071
PMCPMC12480772

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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.