Key result
Shared gene analysis links metabolic pathways and synaptic connections to co-occurring AF and COPD.
Why the study?
AF and COPD co-occurrence is linked to increased morbidity and mortality, but their underlying shared molecular mechanisms remain incompletely analyzed.
This bioinformatic analysis reveals shared gene expression patterns between atrial fibrillation and COPD, suggesting that metabolic processes, synaptic connections, and specific hub genes (such as ALDOC, HNRNPL, and NDUFS2) may play a role in their co-occurrence.
These shared pathways remain hypothesis-generating; leaves open validation of hub genes as biomarkers or targets in prospective studies.
Background: The underlying molecular processes of atrial fibrillation (AF) and chronic obstructive pulmonary disease (COPD) are frequently linked to increased morbidity and mortality when they co-occur. However, their underlying molecular mechanisms are questioned due to their incomplete analysis. Objective: This study aimed to identify common differentially expressed genes (DEGs) in AF and COPD patients and investigate their potential biological functions and pathways. We hope to complement and update previous research through clearer figure presentation and different bioinformatic analysis methods with different datasets. Methods: We used statistical analysis to identify DEGs in the expression profiles of AF and COPD patients using datasets from the Gene Expression Omnibus database. To ascertain whether the common DEGs were functionally enriched, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were used. In addition, we generated protein‒protein interaction networks and identified significant hub genes. Furthermore, the hub genes were used to analyze transcription factor (TF)-gene interactions and TF-miRNA coregulatory networks, and their expression levels were validated in additional datasets. Results: We identified a total of 15 DEGs that were upregulated, whereas 36 were downregulated in AF and COPD patients. The DEGs were commonly expressed in both AF and COPD patients, with functional enrichment analysis revealing their involvement in metabolic processes and neuron-to-neuron synapses. We identified significant hub genes, including TGM2, ITPR1, CHL1, ALDOC, RPS3, FBLN2, NDUFS2, ITGA5, CTNNB1, RBP1, CLSTN2, FABP5, EPHA4, LDHA, and HNRNPL, and analyzed their coexpression and biological functions. TF-gene interaction and TF-miRNA coregulatory network analyses revealed the regulatory relationships of the hub genes. Additional datasets were analyzed to validate hub gene expression, and ALDOC, HNRNPL, and NDUFS2 displayed similar processes in AF and COPD patients. Conclusions: In our study, we demonstrate that metabolic processes and neuron-to-neuron synaptic connections may contribute to the cooccurrence of AF and COPD. The identified hub genes and regulatory networks may act as potential biomarkers and therapeutic targets for these diseases.
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Xiong et al. (2023) studied Atrial fibrillation and chronic obstructive pulmonary disease (n=242). Co-occurrence of atrial fibrillation and chronic obstructive pulmonary disease vs. Sinus rhythm and control smokers was evaluated on Identification of common differentially expressed genes (DEGs). Bioinformatic analysis identified 51 common differentially expressed genes (15 upregulated, 36 downregulated) and 15 hub genes, implicating metabolic processes and synaptic connections in the co-occurrence of AF and COPD.
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