Molecular medicine (Cambridge, Mass.) · 2025
Identifying nexilin as a central gene in neutrophil-driven abdominal aortic aneurysm pathogenesis.
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Yang Bohan, Xu Yiyan, Yan Fengfei, Peng Cheng, Song Ye, Han Song, Wang Haiyang
Аннотация
OBJECTIVES: Abdominal aortic aneurysm (AAA) is an inflammation-driven disease in which neutrophil infiltration is critical to its progression. This study aims to explore the molecular mechanisms behind neutrophil infiltration in AAA and identify key regulatory genes.
METHODS: We utilized weighted gene co-expression network analysis (WGCNA) and differential gene expression analysis to compare AAA and healthy abdominal aortic tissues. Functional enrichment analysis and a protein-protein interaction (PPI) network were constructed to understand gene functions. Machine learning algorithms were applied to identify key hub genes, followed by in vivo validation using an ApoE-/- mouse model.
RESULTS: Neutrophils, NK cells, and pDCs were significantly increased in AAA tissues. WGCNA identified 234 genes associated with neutrophil infiltration, of which 39 were significantly differentially expressed. Functional enrichment analysis highlighted roles in actin-related processes and pathways. Nexilin (NEXN) was consistently identified as a key hub gene negatively correlated with immune cell infiltration. In vivo validation confirmed that NEXN inhibits AAA progression in ApoE-/- mice by regulating immune cell infiltration.
CONCLUSION: NEXN plays a crucial role in modulating neutrophil infiltration in AAA. These findings provide new molecular insights into AAA pathogenesis and suggest NEXN as a potential target for AAA therapy.
METHODS: We utilized weighted gene co-expression network analysis (WGCNA) and differential gene expression analysis to compare AAA and healthy abdominal aortic tissues. Functional enrichment analysis and a protein-protein interaction (PPI) network were constructed to understand gene functions. Machine learning algorithms were applied to identify key hub genes, followed by in vivo validation using an ApoE-/- mouse model.
RESULTS: Neutrophils, NK cells, and pDCs were significantly increased in AAA tissues. WGCNA identified 234 genes associated with neutrophil infiltration, of which 39 were significantly differentially expressed. Functional enrichment analysis highlighted roles in actin-related processes and pathways. Nexilin (NEXN) was consistently identified as a key hub gene negatively correlated with immune cell infiltration. In vivo validation confirmed that NEXN inhibits AAA progression in ApoE-/- mice by regulating immune cell infiltration.
CONCLUSION: NEXN plays a crucial role in modulating neutrophil infiltration in AAA. These findings provide new molecular insights into AAA pathogenesis and suggest NEXN as a potential target for AAA therapy.