Evidence map›Paper›PMID 41230144›Full record

ArticleTranslational andrology and urology2025

Integrated transcriptomics, proteomics, and metabolomics to uncover inflammatory-metabolic crosstalk and key molecules in a mouse model of hyperoxaluria-induced kidney injury.

Bangyu Zou, Meng Shu, Chaoyue Lu, Yiying Jia, Shuwei Zhang, Dongxiang Zhang, Zhaoxin Ying, Ziyu Fang, Yonghan Peng, Xiaofeng Gao

Abstract read
In one paragraph

Article in Translational andrology and urology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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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

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Bangyu Zou *Department of Urology, Changhai Hospital, Naval Medical University, Shanghai, China.ORCID https://orcid.org/0000-0002-0453-1680
Meng Shu *Department of Urology, Changhai Hospital, Naval Medical University, Shanghai, China.
Chaoyue Lu *Department of Urology, Changhai Hospital, Naval Medical University, Shanghai, China.
Yiying JiaDepartment of Urology, Changhai Hospital, Naval Medical University, Shanghai, China.
Shuwei ZhangDepartment of Urology, Changhai Hospital, Naval Medical University, Shanghai, China.
Dongxiang ZhangDepartment of Urology, Changhai Hospital, Naval Medical University, Shanghai, China.
Zhaoxin YingDepartment of Urology, Changhai Hospital, Naval Medical University, Shanghai, China.
Ziyu FangDepartment of Urology, Changhai Hospital, Naval Medical University, Shanghai, China.
Yonghan PengDepartment of Urology, Changhai Hospital, Naval Medical University, Shanghai, China.
Xiaofeng GaoDepartment of Urology, Changhai Hospital, Naval Medical University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Hyperoxaluria, including primary and secondary hyperoxaluria, induces renal tubular damage, interstitial inflammation. This study aimed to elucidate the molecular mechanisms underlying hyperoxaluria-induced kidney injury by integrating multi-omics analyses in a glyoxylate-induced mouse model, focusing on transcriptomic, proteomic, and metabolomic alterations. Methods: Male C57BL/6J mice were divided into control and glyoxylate-treated groups. Kidney tissues were analyzed using transcriptomics, proteomics, and untargeted metabolomics. Histopathology, biochemical assays, and quantitative real-time polymerase chain reaction (qRT-PCR) validation were performed to confirm model establishment and molecular findings. Results: Glyoxylate administration induced calcium oxalate (CaOx) crystal deposition, tubular injury, and elevated serum blood urea nitrogen (BUN) and creatinine (CRE) levels. Transcriptomics revealed 5,099 differentially expressed genes (DEGs), with upregulated inflammatory pathways and downregulated metabolic processes. Proteomics identified 2,966 differentially expressed proteins (DEPs), showing downregulation of fatty acid metabolism pathways and suppressed peroxisomal functions. Metabolomics identified 255 differentially expressed metabolites (DEMs), highlighting disruptions in lipid and amino acid metabolism. Integrative analysis uncovered key gene-metabolite networks. qRT-PCR validated DEGs, including Conclusions: This multi-omics study uncovers interconnected gene, protein, and metabolic changes, highlighting the interplay between inflammation, energy metabolism, and tubular injury in hyperoxaluria-induced kidney injury, and provides novel molecular insights for diagnostic and therapeutic targets.

Indexed as

Calcium oxalate (CaOx)hyperoxaluriametabolomicsproteomicstranscriptomics

Identifiers

PMID41230144
PMCPMC12603837

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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.