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Integrative Multi-Omics and Machine Learning Identify ID1 as a Candidate Gene Associated with Abdominal Aortic
Feng Guo1, Michael Keese2, Yu Zhao1
1Department of Vascular Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Current Issues in Molecular Biology
|February 27, 2026
Summary
Investigating the role of ID1 in abdominal aortic aneurysm (AAA), this study found low ID1 expression is linked to immune cell changes and extracellular matrix remodeling, suggesting ID1 as a potential therapeutic target.
Area of Science:
- Vascular Biology
- Immunology
- Genomics
Background:
- Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease characterized by immune system imbalance and extracellular matrix (ECM) breakdown.
- The precise molecular drivers of AAA pathogenesis remain incompletely understood.
Purpose of the Study:
- To elucidate the mechanistic role of ID1 in the development of AAA.
- To identify potential molecular targets for AAA intervention using multi-omics and machine learning.
Main Methods:
- Integrative analysis of two bulk transcriptomic datasets (GSE232911, GSE183464) using differential expression, WGCNA, and machine learning (LASSO, Random Forest, SVM-RFE).
- Immune infiltration analysis was performed using ssGSEA and CIBERSORT.
- Validation of findings using single-cell RNA sequencing data (GSE226492).
Main Results:
- ID1 was consistently identified as a significantly downregulated gene in AAA across independent datasets, demonstrating strong discriminatory ability (AUC = 0.939 and 0.868).
- Low ID1 expression correlated with heightened adaptive immune responses, increased M1 macrophages, γδ T cells, and memory B cells, alongside reduced neutrophil and mast cell activity.
- Single-cell analysis confirmed ID1 downregulation specifically in endothelial and fibroblast cells within AAA tissues.
Conclusions:
- ID1 is identified as a key candidate gene implicated in the vascular immune remodeling and ECM-related pathways characteristic of AAA.
- The findings provide a foundation for further research into the specific molecular mechanisms of ID1 in AAA pathogenesis and its potential as a therapeutic target.
