Evidence map›Paper›PMID 40806550›Full record

ArticleInternational journal of molecular sciences2025

Identification of Differentially Expressed Genes and Pathways in Non-Diabetic CKD and Diabetic CKD by Integrated Human Transcriptomic Bioinformatics Analysis.

Clara Barrios, Marta Riera, Eva Rodríguez, Eva Márquez, Jimena Del Risco, Melissa Pilco, Jorge Huesca, Ariadna González, Claudia Martyn, Jordi Pujol and 2 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 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

12 authors.

Clara BarriosDepartment of Nephrology, Hospital del Mar, 08003 Barcelona, Spain.
Marta RieraHospital del Mar Research Institute, 08003 Barcelona, Spain.ORCID 0000-0003-4362-7965
Eva RodríguezDepartment of Nephrology, Hospital del Mar, 08003 Barcelona, Spain.
Eva MárquezDepartment of Nephrology, Hospital del Mar, 08003 Barcelona, Spain.
Jimena Del RiscoDepartment of Nephrology, Hospital del Mar, 08003 Barcelona, Spain.
Melissa PilcoDepartment of Nephrology, Hospital del Mar, 08003 Barcelona, Spain.
Jorge HuescaDepartment of Nephrology, Hospital del Mar, 08003 Barcelona, Spain.ORCID 0009-0002-0157-1844
Ariadna GonzálezDepartment of Nephrology, Hospital del Mar, 08003 Barcelona, Spain.
Claudia MartynHospital del Mar Research Institute, 08003 Barcelona, Spain.
Jordi PujolHospital del Mar Research Institute, 08003 Barcelona, Spain.ORCID 0009-0005-8539-2203
Anna BuxedaDepartment of Nephrology, Hospital del Mar, 08003 Barcelona, Spain.ORCID 0000-0001-7305-3259
Marta CrespoDepartment of Nephrology, Hospital del Mar, 08003 Barcelona, Spain.ORCID 0000-0001-6992-6379

Funding

Instituto de Salud Carlos III PI22/00006Instituto de Salud Carlos III RD24/0004/0003
6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a heterogeneous condition with various etiologies, including type 2 diabetes mellitus (T2D), hypertension, and autoimmune disorders. Both diabetic CKD (CKD_T2D) and non-diabetic CKD (CKD_nonT2D) share overlapping clinical features, but understanding the molecular mechanisms underlying each subtype and distinguishing diabetic from non-diabetic forms remain poorly defined. To identify differentially expressed genes (DEGs) and enriched biological pathways between CKD_T2D and CKD_nonT2D cohorts, including autoimmune (CKD_nonT2D_AI) and hypertensive (CKD_nonT2D_HT) subtypes, through integrative transcriptomic analysis. Publicly available gene expression datasets from human glomerular and tubulointerstitial kidney tissues were curated and analyzed from GEO and ArrayExpress. Differential expression analysis and Gene Set Enrichment Analysis (GSEA) were conducted to assess cohort-specific molecular signatures. A considerable overlap in DEGs was observed between CKD_T2D and CKD_nonT2D, with CKD_T2D exhibiting more extensive gene expression changes. Hypertensive-CKD shared greater transcriptomic similarity with CKD_T2D than autoimmune-CKD. Key DEGs involved in fibrosis, inflammation, and complement activation-including

Indexed as

Computational BiologyDiabetes Mellitus, Type 2Diabetic NephropathiesRenal Insufficiency, ChronicTranscriptomeGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksHumansdiabetic chronic kidney diseasedifferential expression analysisgene set enrichment analysisnon-diabetic chronic kidney diseasetranscriptomics

Identifiers

PMID40806550
PMCPMC12347806

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.