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Genetic and Molecular Relationships Between Chronic Obstructive Pulmonary Disease and Abdominal Aortic Aneurysm: Insights from a Multi-Omics Approach

Jian WangSchool of Chemical Engineering, Ocean Technology and Life Science , Dalian University of Technology , Panjin 124221 , ChinaYuemeng LiDepartment of Vascular Surgery , Central Hospital of Dalian University of Technology , Dalian , ChinaYun LiDepartment of Family Medicine , People's Hospital of Tacheng Prefecture , Tacheng , ChinaJamol UzokovRepublican Specialized Scientific Practical Medical Center of Therapy and Medical Rehabilitation , Tashkent , UzbekistanZhaoxuan ZhangSchool of Chemical Engineering, Ocean Technology and Life Science , Dalian University of Technology , Panjin 124221 , ChinaXiaoxu ZhangDeying JiangDepartment of Vascular Surgery , Central Hospital of Dalian University of Technology , Dalian , ChinaHan JiangChina Medical UniversityAzad HussainDepartment of Mathematics , University of Gujrat , Gujrat , PakistanChen ChenSchool of Biomedical Sciences , The University of Queensland , Brisbane , AustraliaJian ZhangDepartment of Vascular Surgery , The First Hospital of China Medical University , Shenyang , ChinaYanshuo HanDepartment of Vascular Surgery , Central Hospital of Dalian University of Technology , Dalian , China

2025en

Ochiq kirishOlmos

Litsenziya: cc-by

ABI

Annotatsiya

Background: Chronic obstructive pulmonary disease (COPD) and abdominal aortic aneurysm (AAA) are both severe conditions with complex etiologies and substantial comorbidities. Previous studies have suggested a potential relationship between these diseases, but the underlying genetic and molecular mechanisms remain unclear. Methods: We used bidirectional two-sample Mendelian randomization (MR) to investigate the causal relationship between COPD and AAA. Expression quantitative trait loci (eQTL) analysis was performed with GTEx V8 summary statistics for aortic and lung tissues. Single-cell sequencing data from GEO datasets were analyzed to identify differentially expressed genes. Finally, a phenome-wide association study (PheWAS) was conducted to explore the broader implications of identified pathogenic genes. Results: We identified a genetic correlation between COPD and AAA. MR analysis revealed that COPD had a significant causal relationship with AAA (P < 0.05). SMR analysis identified 48 common genes associated with both COPD and AAA. Single-cell sequencing identified key genes, thus suggesting their potential roles as pathogenic factors. PheWAS further supported the pleiotropy and broader effects of these genes on various phenotypes. Conclusion: Our findings demonstrated a significant causal relationship between COPD and AAA. An integrative multi-omics approach provided a comprehensive understanding of the molecular mechanisms underlying these diseases.

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DOI: 10.15212/cvia.2025.0003

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