ArticleExperimental and therapeutic medicine2025
Characterization of moyamoya disease molecular subtypes through disulfidptosis‑related genes and immune landscape analysis.
Article in Experimental and therapeutic medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Genetic architecture of swine inflammation and necrosis syndrome and its genetic correlation with repeated skin damage scores.Journal of animal science · 2026Article
- Molecular and multimodal biomarkers in Moyamoya disease: from pathogenic mechanisms to clinical translation.European journal of medical research · 2026Review
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7 authors.
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Abstract
Moyamoya disease (MMD), a chronic cerebrovascular disorder, is characterized by progressive stenosis of major intracranial arteries. However, the mechanisms underlying the pathological narrowing have remained largely elusive. Disulfidptosis is a new mode of cell death caused by the vulnerability of the actin cytoskeleton to disulfide stress, and proteomic profiling of MMD has revealed that abnormal proliferation of endothelial cells may be induced by upregulation of focal adhesion-related proteins. However, the role of disulfidptosis in MMD has not yet been reported. The Gene Expression Omnibus database was searched for datasets with a sample size of more than six and four microarray datasets (GSE189993, GSE157628, GSE141024 and GSE141022) were downloaded. Based on the expression profiles of DRGs in each sample, MMD was clustered into three discrete molecular subtypes. Differential expression analysis was performed using the R package 'limma' to analyze the differences in gene expression between MMD and controls. Functional enrichment analysis was used to explore the molecular functions and mechanisms of the differentially expressed DRGs in MMD. Based on the results of differential expression analysis, the intersection among four comparison groups, which included C1 vs. C2, C1 vs. C3, C2 vs. C3, and MMD vs. controls, were taken and four hub genes were selected for further study. In addition, the expression and distribution of 22 types of immune cells in each sample was analyzed. Spearman's correlation analysis was performed to explore the correlation between the hub genes and the proportion of immune cells. MMD-related genes were identified and the relationship between them and hub genes was analyzed. Furthermore, ELISA was performed to verify the expression of the four MMD hub genes. In the present study, a novel molecular classification of MMD based on disulfidptosis gene expression was established and a total of 348 upregulated and 801 downregulated genes were identified in patients with MMD compared with controls. A total of four hub genes (
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