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Gene Expression Signatures of Smoking and Acute Myocardial Infarction: A Blood Transcriptome Analysis
Fang-Fang Liu1, Yi-Xuan Yan2, Hong-Feng Zhang1
1Department of Pathology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, China.
Smoking alters blood gene expression, increasing acute myocardial infarction (AMI) risk. Researchers identified key genes in blood that link smoking to AMI, potentially serving as future biomarkers for cardiovascular health.
Area of Science:
- Cardiovascular Disease Research
- Molecular Biology
- Genomics
Background:
- Smoking is a major risk factor for cardiovascular diseases like hypertension and myocardial infarction (MI).
- The exact molecular mechanisms linking smoking to cardiovascular disease remain unclear.
- Understanding these links is crucial for developing preventative and therapeutic strategies.
Purpose of the Study:
- To identify shared molecular signatures in blood that connect smoking exposure to acute myocardial infarction (AMI).
- To investigate the role of gene expression changes in smoking-related cardiovascular risk.
Main Methods:
- Meta-analysis of seven blood transcriptome microarray datasets from the Gene Expression Omnibus (GEO) database (403 patients).
- Identification of differentially expressed genes (DEGs) associated with AMI and smoking.
- Functional enrichment analysis and validation of key genes using independent datasets and qRT-PCR.
Main Results:
- DEGs linked to AMI and smoking were significantly enriched in immune response and inflammation pathways.
- Three genes (PTGDR, PYHIN1, PRSS23) showed consistent alterations in both smoking and AMI.
- PYHIN1 and PRSS23 dysregulation in AMI was confirmed by qRT-PCR.
Conclusions:
- Smoking-induced blood gene expression changes may contribute to AMI risk.
- The identified genes (PTGDR, PYHIN1, PRSS23) are implicated in AMI pathogenesis.
- These genes could serve as blood-based biomarkers for cardiovascular risk assessment in smokers.
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