ArticlePloS one2025
Comprehensive analysis of cuproptosis-related genes in diabetic cardiomyopathy.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic cardiomyopathy (DCM) represents a distinct myocardial pathology arising from chronic diabetic metabolic disturbances, characterized by progressive structural and functional abnormalities that frequently culminate in heart failure. Cuproptosis, a novel form of cell death, is highly linked to mitochondrial metabolism and mediated by protein lipoylation. However, studies are limited on the clinical significance of cuproptosis-related genes (CRGs) in DCM. Therefore, it is helpful to identify CRGs involved in DCM and explore their expression and molecular mechanisms.
methodsWe downloaded three datasets of DCM from the GEO database and a set of cuproptosis-related genes with 176 genes. Following the identification of the differentially expressed cuproptosis-related genes(DECRGs) and hub genes, we performed the functional annotation, protein-protein interaction network, co-expression network analysis, mRNA-miRNA regulatory network.The GSE5606 dataset was then used to verify hub genes. Finally, we validated the expression of hub genes in a high glucose-induced H9C2 cell injury model via RT-qPCR.
resultsWe identified 14 DEFRGs and 7 key genes in the DCM samples compared to the control. Functional enrichment analysis revealed that DECRGs are associated with several pathways, including TCA cycle, respiratory electron transport, oxidative stress, and metabolism pathway. Moreover, Isocitrate dehydrogenase 1(Idh1), Cytochrome P450 Family 1 Subfamily A Member 1(Cyp1a1), 3-Hydroxy-3-Methylglutaryl-CoA Synthase (Hmgcs2) and Hexokinase 2(Hk2) were identified as the hub genes and validated in the GSE5606 datasets with area under the curve(AUC)>0.7. The qRT-PCR results showed that the expression levels of Cyp1a1, Hmgcs2, HK2, and Idh1 in vitro model of DCM and controls were consistent with the bioinformatics analysis results from the mRNA microarray.
conclusionsOverall,we identified hub genes and pathways involved in DCM via bioinformatics analysis and revealed the potential role of cuproptosis, providing useful and novel information to explore the potential candidate genes for DCM diagnostic and therapeutic options.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.