Evidence map›Paper›PMID 40258914›Full record

ArticleScientific reports2025

Integrated multiomics analysis identifies potential biomarkers and therapeutic targets for autophagy associated AKI to CKD transition.

Yaojun Wang, Qiang Li

Abstract read
In one paragraph

Article in Scientific reports, 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. Review
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

2 authors.

Yaojun WangClinical Medical College, Affiliated Hospital, Hebei University, Baoding, 071000, Hebei, China.
Qiang LiDepartment of Dermatology, Air Force Medical Center, PLA, Beijing, 100142, China. 16585260@qq.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study explored the relationship between acute kidney injury (AKI) and chronic kidney disease (CKD), focusing on autophagy-related genes and their immune infiltration during the transition from AKI to CKD. We performed weighted correlation network analysis (WGCNA) using two microarray datasets (GSE139061 and GSE66494) in the GEO database and identified autophagy signatures by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), and GSEA enrichment analysis. Machine learning algorithms such as LASSO, random forest, and XGBoost were used to construct the diagnostic model, and the diagnostic performance of GSE30718 (AKI) and GSE37171 (CKD) was used as validation cohorts to evaluate its diagnostic performance. The study identified 14 autophagy candidate genes, among which ATP6V1C1 and COPA were identified as key biomarkers that were able to effectively distinguish between AKI and CKD. Immune cell infiltration and GSEA analysis revealed immune dysregulation in AKI, and these genes were associated with inflammation and immune pathways. Single-cell analysis showed that ATP6V1C1 and COPA were specifically expressed in AKI and CKD, which may be related to renal fibrosis. In addition, drug prediction and molecular docking analysis proposed SZ(+)-(S)-202-791 and PDE4 inhibitor 16 as potential therapeutic agents. In summary, this study provides new insights into the relationship between AKI and CKD and lays a foundation for the development of new treatment strategies.

Indexed as

Acute Kidney InjuryAutophagyBiomarkersRenal Insufficiency, ChronicGene Expression ProfilingGene OntologyGene Regulatory NetworksHumansMolecular Docking SimulationMultiomicsBiomarkersAKI; CKDAutophagyBiomarkersMachine learning

Identifiers

PMID40258914
PMCPMC12012120

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.