Evidence map›Paper›PMID 39044690›Full record

ArticleHistology and histopathology2025

Bioinformatics study of the TNFRSF1A mechanism involved in acute liver injury in sepsis through the mTOR signaling pathway.

Zhidong Chen, Kankai Tang, Hui Zhang

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Article in Histology and histopathology, 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
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1citing papers in PubMed
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1 · What the graph read from it

What it found

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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.

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Zhidong ChenDepartment of Intensive Care Unit, the First Affiliated Hospital of Huzhou University, Huzhou, Zhejiang Province, China.
Kankai TangDepartment of Intensive Care Unit, the First Affiliated Hospital of Huzhou University, Huzhou, Zhejiang Province, China.
Hui ZhangDepartment of Anesthesiology, the First Affiliated Hospital of Huzhou University, Huzhou, Zhejiang Province, China. zhanghui_hzyy@163.com.

Funding

The public welfare technology application research program of Huzhou 2021GZ72
6 · The paper itself

Abstract

objectivesThis study analyzed potential key genes involved in the mechanism of acute liver injury induced by sepsis through bioinformatics techniques, aiming to provide novel insights for the identification of early-stage sepsis-induced acute liver injury and its diagnosis.

methodsGene chip data sets containing samples from acute liver injury induced by sepsis and control groups (GSE22009 and GSE60088) were selected from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) with |log fold change| >1 and

resultsA total of 646 upregulated DEGs were determined in GSE22009 and 146 in GSE60088. A Venn diagram was used to find the intersection of the upregulated DEGs between the two data sets, and 67 DEGs associated with sepsis-mediated acute liver damage were obtained. Enrichment analysis from the KEGG pathway showed that DEG upregulation was primarily associated with various pathways: TNF, NF-κB, IL-17, ferroptosis, mTOR, and JAK-STAT signaling pathways. DEGs resulted in three clusters and 15 candidate genes, as revealed by the PPI network and module analyses. Intersection with sepsis-induced acute liver injury-related genes in the CTD resulted in the identification of three significant differentially co-expressed genes:

conclusionThe key genes identified and related signaling pathways provided insights into the molecular mechanisms of sepsis-induced acute liver injury. In vivo studies revealed the overexpression of

Indexed as

Receptors, Tumor Necrosis Factor, Type ISepsisTOR Serine-Threonine KinasesAnimalsComputational BiologyDisease Models, AnimalGene Expression ProfilingLiverMaleProtein Interaction MapsRatsRats, Sprague-DawleySignal TransductionmTOR protein, ratReceptors, Tumor Necrosis Factor, Type ITnfrsf1a protein, ratTOR Serine-Threonine Kinases

Identifiers

PMID39044690

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