ArticleFrontiers in immunology2025
Integrated proteomics and single-cell transcriptomics reveal potential therapeutic targets in Wilson's disease patients.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Wilson's Disease (WD), an autosomal recessive Methods: Proteomic analysis was conducted on clinical samples from WD patients and the control group, followed by validation via ELISA. Subsequently, an integrated analysis was conducted by combining these data with single-cell RNA sequencing data from the database. Analytical content included differential expression, functional enrichment, drug target prediction, immune infiltration, and subtype-specific biomarker screening via LASSO/SVM-REF. Results: Proteomic analysis identified 420 differentially expressed proteins (266 upregulated, 154 downregulated) in WD patients compared with healthy controls, with significant enrichment in inflammatory pathways. Integration with DrugBank revealed eight hub proteins with high diagnostic accuracy (AUC > 0.9), among which Inter-alpha-trypsin inhibitor heavy chain 1 (ITIH1) and Transthyretin (TTR) may regulate the PI3K-Akt signaling pathway. Subsequently, ELISA validation confirmed significantly reduced levels of TTR, Ceruloplasmin (CP), and ITIH1 proteins in WD. Considering the heterogeneity of the WD microenvironment and single-cell diversity, further single-cell transcriptomic analysis was performed. The results revealed immune dysregulation, characterized by increased macrophage infiltration and reduced T/NK cell proportions, and PI3K-Akt-mTOR pathway enrichment in macrophages. For subtype-specific analysis, six key proteins were identified to distinguish hepatic and brain subtypes (AUC > 0.9). Conclusions: The hub proteins and subtype-specific biomarkers identified in this study provide potential targets for the precise treatment of WD, while emphasizing the critical role of the PI3K-Akt pathway in WD.
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.