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Construction and Analysis of Immune Infiltration and Competing Endogenous RNA Network in Moyamoya Disease
Construction and Analysis of Immune Infiltration and Competing Endogenous RNA Network in Moyamoya Disease
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Construction and Analysis of Immune Infiltration and Competing Endogenous RNA Network in Moyamoya Disease
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Construction and Analysis of Immune Infiltration and Competing Endogenous RNA Network in Moyamoya Disease
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Construction and Analysis of Immune Infiltration and Competing Endogenous RNA Network in Moyamoya Disease
Construction and Analysis of Immune Infiltration and Competing Endogenous RNA Network in Moyamoya Disease
Journal Article

Construction and Analysis of Immune Infiltration and Competing Endogenous RNA Network in Moyamoya Disease

2025
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Overview
Moyamoya disease (MMD) is a cerebrovascular condition characterized by progressive stenosis of intracranial arteries, leading to stroke. While MMD was long considered a genetic disorder, emerging evidence suggests autoimmune mechanisms may contribute to its pathogenesis. The role of non-coding RNAs (ncRNAs) in the pathogenesis of MMD is under heated discussion, and a competitive endogenous RNA (ceRNA) network involving MMD-related ncRNAs has not been constructed. In this study, we integrated multiple bioinformatic analyses on transcriptomic data from the middle cerebral arteries of MMD patients and controls. Our analysis revealed a significant enrichment of innate immune system pathways, including antigen processing and macrophage activation, in MMD tissue. We constructed a robust ceRNA network centered on the long non-coding RNA MALAT1, identifying 15 core mRNA targets. A classifier built from these MALAT1-related genes accurately distinguished MMD patients from controls, with an area under the curve of 0.869 in independent validation. Furthermore, immune deconvolution analysis showed a marked increase in microvascular endothelial cells and a decrease in CD4+ memory T cells and regulatory T cells in MMD arteries. The expression of the MALAT1 network genes strongly correlated with these shifts in cellular composition, positively with endothelial cells and negatively with T cells. Our findings uncover a MALAT1-driven ceRNA network that links immune dysregulation to vascular changes in MMD, highlighting MALAT1 as a potential biomarker and therapeutic target.