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Updated: May 10, 2025

Author Spotlight: Enhanced Murine AAA Model Using Elastase to Mimic Human Aneurysms
Published on: July 26, 2024
Revealing shared molecular and mechanistic signatures between intracranial aneurysms and abdominal aortic aneurysms:
Xiao Liu1,2, Zhenjun Li3, Hongzhen Xu4
1Department of Neurosurgery, The Engineering Technology Research Center of Education Ministry of China, Guangdong Provincial Key Laboratory On Brain Function Repair and Regeneration, The Neurosurgery Institute of Guangdong Province, Zhujiang Hospital, Southern Medical University, The National Key Clinical Specialty, Guangzhou, 510282, China.
Abstract:
Intracranial aneurysms (IAs) and abdominal aortic aneurysms (AAAs) are both vascular diseases that are closely linked. However, the pathogenesis underlying the co-occurrence of IAs and AAAs remains poorly understood. This study aims to identify key biomarkers that shed light on the molecular mechanisms connecting these two diseases using bioinformatics analysis. Gene expression profiles (GSE122897, GSE237229) were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) common to both IAs and AAAs were identified and subjected to functional enrichment analysis. The Cytoscape cytoHubba plugin was used to identify hub genes, and their predictive ability was evaluated using the receiver operating characteristic (ROC) curve. Additionally, immune infiltration analyses and single-gene gene set enrichment analysis (GSEA) were conducted for the hub genes. A total of 46 DEGs were identified, including 40 upregulated genes and 6 downregulated genes. The common DEGs were found to be involved in extracellular matrix structural constituents, collagen fibril organization, and regulation of basic cellular processes. ITGA11 was identified as a key gene implicated in the comorbidity of IAs and AAAs, with its upregulation strongly associated with plasma cells. Furthermore, in both IAs and AAAs, glycosaminoglycan biosynthesis of extracellular matrix components and immune-related diseases were significantly linked to the high expression of ITGA11. Our findings suggest that the comorbidity of IAs and AAAs may be driven by shared inflammatory and immune response mechanisms, with ITGA11 emerging as a potential biomarker for this co-occurrence.

