Evidence map›Paper›PMID 40155864›Full record

ArticleBMC nephrology2025

Novel insights into the molecular mechanisms of sepsis-associated acute kidney injury: an integrative study of GBP2, PSMB8, PSMB9 genes and immune microenvironment characteristics.

Haiting Ye, Xiang Zhang, Pengyan Li, Mei Wang, Ruolan Liu, Dingping Yang

Abstract read
In one paragraph

Article in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

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0cells of the map it votes in
4citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Haiting YeDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China.
Xiang ZhangDepartment of Clinical Laboratory, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Pengyan LiDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China.
Mei WangDepartment of Transfusion, Wuhan Third Hospital (Tongren Hospital of Wuhan University), Wuhan, China.
Ruolan LiuDepartment of Transfusion, Wuhan Third Hospital (Tongren Hospital of Wuhan University), Wuhan, China.
Dingping YangDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China. shenbinneike@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSepsis-associated acute kidney injury (SA-AKI) is a prevalent and severe complication of sepsis, but its complex pathogenesis remains unclear. This study aims to identify potential biomarkers for SA-AKI by elucidating its molecular mechanisms through bioinformatics methods.

methodsTranscriptional data related to SA-AKI were obtained from the Gene Expression Omnibus (GEO) database. We used differentially expressed genes (DEGs) and weighted gene co-expression network analysis (WGCNA) to identify characteristic genes associated with SA-AKI and conducted enrichment analyses. Hub genes were determined using protein-protein interaction (PPI) network analysis and the Least Absolute Shrinkage and Selection Operator (LASSO). Additionally, ROC curves were plotted to assess the diagnostic value of these core genes. Immune cell infiltration was analyzed using the CIBERSORT algorithm, and potential associations between the hub genes and clinicopathological features were explored based on the Nephroseq database. Finally, a murine model of SA-AKI was induced with lipopolysaccharide (LPS) to validate the findings, and mRNA abundance and protein production levels of pivotal genes were confirmed via RT-qPCR, Western blotting, and immunohistochemical methods.

resultsWe identified 268 characteristic genes associated with SA-AKI that are enriched in immune and inflammation-related pathways. Utilizing machine learning techniques, three key genes were screened: GBP2, PSMB8 and PSMB9. The expression patterns of these three genes were well-validated through animal experiments and databases. Correlation between these genes and clinical indicators was confirmed using the Nephroseq database. Furthermore, immune infiltration analysis provided additional insights into their potential functions.

conclusionGBP2, PSMB8, and PSMB9 are promising candidate genes for SA-AKI, providing a novel perspective on its pathological mechanisms. Further exploration of the biological roles of these genes in the pathogenesis of SA-AKI is needed in the future.

Indexed as

Acute Kidney InjuryProteasome Endopeptidase ComplexSepsisAnimalsHumansMaleMiceMice, Inbred C57BLProtein Interaction MapsLMP7 proteinProteasome Endopeptidase ComplexBioinformaticsImmune infiltrationLASSOSepsis-associated acute kidney injuryWGCNA

Identifiers

PMID40155864
PMCPMC11954279

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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.