ArticlePloS one2025
Cuproptosis-related genes associated with mitochondrial dysfunction in Parkinson's disease.
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.
- Nrf2 Activators in Parkinson's Disease: Modulating Mitophagy and Regulating Cuproptosis.Molecular neurobiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD), a neurodegenerative condition characterized by the loss of dopamine neurons and motor deficits, has recently been associated with cuproptosis, a process potentially leading to mitochondrial dysfunction. This study utilized six PD datasets from the GEO database, designating one for internal training and the remaining five for external validation. Various analytical methods, such as Gene Set Enrichment Analysis (GSEA), immune infiltration studies, and differential expression analysis, were employed to pinpoint differentially expressed genes (DEGs). The research also applied Weighted Gene Co-expression Network Analysis (WGCNA) to identify module genes, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. By intersecting DEGs with cuproptosis-related genes (CRGs), differentially expressed cuproptosis-related genes (DECRGs) were identified and assessed using Receiver Operating Characteristic (ROC) curves. Further analysis led to the discovery of differentially expressed cuproptosis-mitochondrial dysfunction-related genes (DEC-MDRGs), which were validated and subjected to additional scrutiny. The study concluded with predictions of potential therapeutic drugs. The findings revealed 6685 DEGs and 31 distinct modules, with gene functions predominantly enriched in immune-related pathways. Twelve DECRGs, recognized as high-diagnostic-potential hub genes (AUC > 0.9), were identified for early PD diagnosis. Additionally, eight DEC-MDRGs were found to be expressed across various neural cells. The miRNA network highlighted the significance of miR-4632 and miR-637. In a MPTP-induced mouse model of PD, differential gene expression was confirmed through gene and protein analysis. Transmission electron microscopy (TEM) uncovered mitochondrial alterations in SH-SY5Y cells. Potential PD treatments, including NADH, Radicipol, and Glycine, were also identified. In summary, advancements in PD prevention, diagnosis, and treatment can be achieved by modulating copper metabolism and mitochondrial function, thereby enhancing the quality of life for patients.
Indexed as
Identifiers
What Socratic 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 Socratic graph.