ArticleVascular health and risk management2025
Linking Cellular Senescence to Vascular Pathology: The Diagnostic Potential of Superoxide Dismutase 2 in Aortic Dissection.
Article in Vascular health and risk management, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: This study investigates the molecular and cellular mechanisms of vascular aging and its critical role in the pathogenesis of aortic dissection (AD), employing an integrative approach that includes bioinformatics and single-cell transcriptomic analyses. Methods: Differentially expressed genes (DEGs) were identified from publicly available datasets (GSE52093, GSE153434), with 194 upregulated and 518 downregulated genes, 16 of which were associated with vascular aging. Superoxide dismutase 2 (SOD2) was identified as a critical gene, demonstrating significant diagnostic accuracy for AD through ROC analysis. Single-cell RNA sequencing of AD tissues revealed cellular heterogeneity, with a predominant macrophage infiltration and altered proportions of endothelial and smooth muscle cells. Results: SOD2 was notably expressed in macrophages and dendritic cells, particularly in AD tissues, suggesting its involvement in immune modulation. Validation of SOD2 at both mRNA and protein levels showed elevated expression in AD tissues and serum, correlating with increased oxidative stress and immune cell infiltration. Elevated serum SOD2 levels were linked to poor clinical outcomes, particularly higher in-hospital mortality. Immune profiling further identified significant associations between SOD2 and macrophage activity. Conclusion: These findings suggest SOD2 as a potential diagnostic biomarker and therapeutic target for AD. A gene-drug interaction network proposed pharmacological candidates for SOD2 modulation, paving the way for targeted therapies. This study advances the understanding of AD pathogenesis, emphasizing the interplay between oxidative stress, immune response, and vascular aging at both molecular and cellular levels.
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